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Basophil Percentage Of Leukocytes

Basophil percentage of leukocytes, often referred to as basophil percentage or BASO%, represents the proportion of basophils among the total white blood cells (leukocytes) in a blood sample. This metric is a standard component of a complete blood count (CBC) and serves as an indicator of immune system status and overall health. Variations in this percentage can reflect underlying physiological processes, immune responses, or pathological conditions.

Basophils are the least numerous type of granulocyte, a category of white blood cells characterized by the presence of granules in their cytoplasm. They originate from hematopoietic stem cells (HSCs) in the bone marrow, differentiating through common myeloid progenitor (CMP) and granulocyte macrophage progenitor (GMP) stages.[1]Though scarce, basophils play a crucial role in the immune system, particularly in mediating allergic reactions, inflammation, and responses to parasitic infections. They release potent chemical mediators, such as histamine and heparin, from their granules upon activation. The precise regulation of basophil production, maturation, and function is complex and influenced by both environmental and genetic factors.[1]

The percentage of basophils in peripheral blood is a tightly controlled biological trait. Genetic factors are known to contribute significantly to the inter-individual variation observed in basophil percentage and other blood cell traits.[1]Genome-wide association studies (GWAS) have identified numerous genetic variants that influence these traits, including basophil percentage.[1] These genetic influences can affect not only the typical (mean) levels of basophils but also the variability (variance) of the trait within populations.[2]Understanding the genetic architecture underlying basophil percentage provides insights into the molecular pathways governing immune cell development and function.

The basophil percentage is a valuable diagnostic and monitoring tool in clinical practice. Abnormal levels can signal a range of health issues:

  • Basophilia (elevated basophil percentage):This can be associated with allergic reactions (e.g., asthma, hay fever, food allergies), chronic inflammatory conditions, parasitic infections, hypothyroidism, and certain myeloproliferative disorders like chronic myeloid leukemia.
  • Basopenia (decreased basophil percentage):While less common, low basophil levels may be observed in acute infections, hyperthyroidism, and severe stress reactions. As part of routine health check-ups, the basophil percentage helps clinicians assess immune function and detect potential health problems early.[3]Furthermore, research has established links between variations in blood cell traits, including basophil percentage, and susceptibility to common complex diseases, such as autoimmune, cardiometabolic, and neuropsychiatric conditions.[1]

The routine measurement of basophil percentage, alongside other blood cell parameters, is a cornerstone of modern healthcare, enabling widespread screening and diagnosis. Advances in understanding the genetic determinants of basophil percentage hold significant social importance. By identifying specific genetic variants that influence this trait, researchers can improve risk prediction for various immune-related conditions and potentially develop more personalized diagnostic and therapeutic strategies. This knowledge contributes to a broader understanding of human biology, disease pathogenesis, and the development of precision medicine approaches to health management.

Methodological and Statistical Considerations

Section titled “Methodological and Statistical Considerations”

Understanding the genetic influences on basophil percentage of leukocytes is subject to several methodological and statistical constraints. Studies, while often leveraging large sample sizes through meta-analyses of cohorts such as UK Biobank, UK BiLEVE, and INTERVAL.[1] require extensive adjustments for technical and non-genetic biological variations. Technical factors like the time elapsed between blood draw and analysis, instrument drift, and calibration events can account for a substantial portion of the trait’s variance.[1] Furthermore, significant non-technical factors, including age, sex, and menopausal status, can explain up to 40% of the variance, necessitating sophisticated and flexible adjustment models to accurately identify genetic associations.[1] The integration of data from different studies, which may employ “different models of hematology analyzer” and distinct “phenotyping measurement techniques,” introduces potential sources of heterogeneity in effect sizes.[1] While methods like “double genomic control” and adjustments for “genomic control inflation factor” are applied to mitigate biases and variance inflation in summary statistics, the underlying complexity of these analytical processes highlights the persistent challenge of accurately quantifying genetic effects.[1] Such variability can complicate the interpretation of findings and the comparability of results across different research endeavors.

Generalizability and Population Specificity

Section titled “Generalizability and Population Specificity”

A significant limitation in the current understanding of basophil percentage of leukocytes stems from constraints in generalizability, primarily due to cohort ancestry. Many large-scale genetic studies, including those by Astle et al., have predominantly focused on populations of European descent.[1] While valuable insights have been gained from these cohorts, and some research has begun to include other ancestries, such as Korean individuals.[3]the genetic architecture underlying basophil percentage can vary considerably across diverse global populations.

Differences in allele frequencies, linkage disequilibrium patterns, and environmental exposures can mean that genetic variants identified in one population may not have the same effect size or even be associated with the trait in another.[1]This specificity limits the direct applicability of current findings to individuals from non-European or non-East Asian backgrounds, underscoring the need for more inclusive and diverse cohorts to fully map the genetic landscape of basophil percentage globally.

Despite comprehensive genetic analyses, the complete etiology of basophil percentage of leukocytes involves complex interactions and retains areas of unexplained variance. Studies acknowledge that “population-genotype interactions” can lead to genuine differences in allelic effect sizes between studies, suggesting that environmental contexts significantly modulate how genetic factors influence basophil percentage.[1] Accurately disentangling these gene-environment confounders remains a considerable challenge, as many environmental influences are difficult to measure comprehensively or integrate into genetic models.

Furthermore, even when genetic associations are robustly identified, the precise biological mechanisms by which these variants impact basophil percentage are often not fully elucidated. For example, colocalization analyses have shown that only a minority of genetic associations in high linkage disequilibrium with molecular events have a high probability of true colocalization, indicating that the functional consequences of many identified variants are yet to be fully understood.[1] This gap highlights the need for continued research to bridge the divide between genetic association and functional causality, thereby enhancing the predictive power and clinical utility of these genetic insights.

Genetic variations play a crucial role in determining the percentage of basophils among leukocytes, a key indicator in immune response and allergic conditions. Several genes, including both protein-coding and non-coding RNAs, harbor variants that influence this trait, often through diverse molecular mechanisms affecting cell development, differentiation, and function. Genome-wide association studies (GWAS) have identified numerous sentinel variants influencing blood cell indices, providing insights into their complex genetic architecture.[1] One significant locus involves the long intergenic non-coding RNA LINC02768, where variants such as rs370718489 , rs6701752 , and rs10803164 have been associated with the variance of basophil percentage of white cells. As a non-coding RNA,LINC02768is believed to regulate gene expression at various levels, impacting the stability or transcription of genes critical for basophil development and function.[2] Such regulatory variants are common drivers of complex traits, often acting by influencing molecular events like gene expression or histone modifications. Additionally, the RPN1 (Ribophorin I) gene, with variants like rs6782812 and rs3829729 , contributes to the genetic landscape. RPN1 is involved in the N-linked glycosylation of proteins in the endoplasmic reticulum, a process essential for the proper folding and function of numerous cell surface receptors and signaling molecules vital for immune cell communication and maturation.

The SLC7A10 - CEBPA locus, encompassing variants like rs78744187 , rs12151289 , and rs34129834 , is particularly relevant. CEBPA (CCAAT Enhancer Binding Protein Alpha) is a well-known transcription factor that acts as a master regulator of myeloid differentiation, a process that gives rise to granulocytes, including basophils. Variants in CEBPA can alter its DNA-binding affinity or expression levels, consequently affecting the differentiation and maturation of myeloid progenitors into basophils, thus directly influencing their percentage in circulation.[1] SLC7A10(Solute Carrier Family 7 Member 10) is an amino acid transporter that can influence cellular metabolism, thereby supporting the growth and differentiation of hematopoietic cells. The geneLARP4B (La Ribonucleoprotein Domain Family Member 4B), represented by rs11253511 , rs12762973 , and rs56318703 , is an RNA-binding protein, suggesting its role in regulating mRNA stability or translation. Variations in LARP4Bcould therefore modulate the expression of proteins crucial for basophil survival, proliferation, or activation.

Further contributing to the genetic architecture of basophil percentage are variants in genes involved in cell signaling, migration, and proliferation.IQGAP1 (IQ Motif And GTPase Activating Protein 1), with variant rs2074585 , functions as a scaffolding protein that integrates various signaling pathways involved in cell adhesion, migration, and cytoskeletal organization, which are fundamental processes for immune cell trafficking and function. LMNB1-DT (Lamin B1 DNA damage-associated transcript), a long non-coding RNA associated with rs2271352 , likely exerts regulatory effects on gene expression, impacting basophil homeostasis. TheP2RY2 (Purinergic Receptor P2Y2) gene, with variants rs74472890 and rs3741156 , encodes a receptor for extracellular nucleotides, playing a role in inflammation and cell activation, which can modulate basophil responses. Moreover,CCR3 (C-C Motif Chemokine Receptor 3), featuring rs3181077 , is a key chemokine receptor highly expressed on basophils and crucial for their recruitment to inflammatory sites, particularly in allergic reactions.[1] ZYX (Zyxin), marked by rs11772895 , is involved in cell adhesion and mechanotransduction, indirectly affecting basophil mobility. Lastly,CDK6 (Cyclin-Dependent Kinase 6), with variants rs445 and rs17696150 , is a cell cycle regulator important for the proliferation and differentiation of hematopoietic progenitor cells, thereby influencing the overall production and number of basophils.

RS IDGeneRelated Traits
rs370718489
rs6701752
rs10803164
LINC02768basophil count
basophil percentage of leukocytes
rs6782812
rs3829729
LINC01565 - RPN1basophil count
eosinophil count
basophil percentage of leukocytes
basophil percentage of granulocytes
neutrophil count
rs78744187
rs12151289
rs34129834
SLC7A10 - CEBPAerythrocyte volume
basophil count, eosinophil count
basophil count
blood protein amount
erythrocyte count
rs11253511
rs12762973
rs56318703
LARP4Bbasophil count
eosinophil count
basophil percentage of leukocytes
rs2074585 IQGAP1basophil count
balding measurement
basophil percentage of leukocytes
basophil percentage of granulocytes
testosterone measurement
rs2271352 LMNB1-DTbasophil count
basophil percentage of leukocytes
basophil percentage of granulocytes
rs74472890
rs3741156
P2RY2basophil count
basophil percentage of leukocytes
basophil percentage of granulocytes
monocyte percentage of leukocytes
monocyte count
rs3181077 CCR3basophil count
narcolepsy-cataplexy syndrome
basophil percentage of leukocytes
basophil percentage of granulocytes
eotaxin measurement
rs11772895 ZYXbasophil count
monocyte count
basophil percentage of leukocytes
monocyte percentage of leukocytes
rs445
rs17696150
CDK6leukocyte quantity
eosinophil count
neutrophil count, eosinophil count
granulocyte count
basophil count

Basophil percentage of leukocytes, often referred to as BASO% or baso_p, represents the proportion of basophils within the total white blood cell (leukocyte) population. Basophils are the least common type of granulocyte, playing a critical role in allergic reactions and immune responses. This specific hematological trait quantifies their relative abundance, providing insights into an individual’s immune status and inflammatory potential . Genome-wide association studies have identified numerous genetic variants that modulate this trait, including 23 independent variance quantitative trait loci (vQTLs) specifically associated with basophil percentage, which indicates that genetic factors affect not only the average level but also the degree of variability in this measure.[2] These genetic contributions often involve a polygenic architecture, where many common variants each contribute small additive effects, and some rare or low-frequency coding variants can also exert notable impacts on phenotype.[1] A notable example is a pleiotropic lead vQTL located in the HBMgene region, which has been associated with the variance of basophil count, highlighting specific genomic areas that play a role in regulating basophil levels.[2]

The regulation of basophil percentage is also intricately shaped by epigenetic mechanisms and early developmental processes. Research indicates that a significant portion of the heritability observed in blood cell traits, including the basophil percentage, can be attributed to regulatory states derived from epigenomic data.[1]This includes the influence of histone modifications, such as H3K4me1 and H3K27ac, which mark enhancers and promoters respectively, thereby affecting gene expression relevant to basophil development and function.[1] Such epigenetic changes, potentially established during early life, contribute to the long-term programming of hematopoietic stem cells and their subsequent differentiation into myeloid lineages, ultimately impacting the circulating percentage of basophils.[1]

Environmental factors and various lifestyle choices play a considerable role in modulating basophil percentage. A wide array of lifestyle variables, including an individual’s smoking history, alcohol consumption, physical exercise levels, coffee intake, and even sleep patterns such as nocturia, are recognized as potential modifiers of hematologic system traits.[3]Beyond personal habits, broader environmental exposures, socioeconomic factors, and geographic location can indirectly influence immune system function and, consequently, basophil levels. Furthermore, the complex interplay between an individual’s genetic predisposition and these environmental triggers, known as gene-environment interactions, can significantly modify the phenotypic expression of basophil percentage, although specific interaction mechanisms for basophils are still under investigation.[1]

Various demographic characteristics and technical aspects of blood sample handling and analysis also contribute to variations in basophil percentage. Non-technical factors such as age, sex, and menopause status are substantial covariates, collectively explaining up to 40% of the variance observed in blood cell indices after accounting for technical adjustments.[1]For instance, physiological changes associated with aging or hormonal shifts linked to sex and menopause can alter basophil production, maturation, or circulation. Additionally, technical covariates, including the time elapsed between venipuncture and subsequent full blood count analysis, instrument calibration, and potential equipment malfunctions, can introduce measurable variability in basophil percentage, accounting for up to 16% of the observed variance.[1]

Basophils are a distinct type of granulocytic white blood cell, representing a small but crucial component of the innate immune system. The basophil percentage of leukocytes, also known as BASO% or baso_p, quantifies their proportion within the total white blood cell population.[1]This measurement serves as an indicator of an individual’s immune status and is part of the comprehensive hematological indices routinely assessed in clinical settings due to their known roles in disease and diagnostic utility.[2]While the specific molecular mechanisms governing all basophil functions are part of the broader, still incompletely understood molecular programs controlling hematopoietic cell differentiation and proliferation, their presence and relative abundance are critical for a balanced immune response.[1]

The genesis of basophils begins with hematopoietic stem cells (HSCs) residing in the bone marrow, which undergo a complex and tightly regulated differentiation process.[1] This developmental pathway involves several progenitor stages, starting from multipotent progenitors (MPP), progressing through common myeloid progenitors (CMP), and then granulocyte-macrophage progenitors (GMP), before culminating in the maturation of basophils.[1] Insights into the molecular pathways and regulatory networks governing this intricate differentiation and proliferation process have traditionally been gleaned from studies of highly penetrant mutations associated with inherited disorders of the hematopoietic system and somatic mutations underlying blood cell cancers.[1] More recently, high-throughput molecular and genetic analyses of common biological variation have significantly advanced the understanding of these complex developmental programs.[1]

The percentage of basophils among leukocytes is a trait significantly influenced by genetic factors, as revealed by genome-wide association studies (GWAS) that have charted its complex allelic landscape.[1]Research indicates that basophil percentage (baso_p) and basophil cell count (baso) are particularly notable for yielding a substantial number of independent variance quantitative trait loci (vQTLs), highlighting a strong genetic influence on the variability of this trait within populations.[2] Many of the genetic variants identified in these studies are non-coding, located in regions such as introns, intergenic spaces, or untranslated regions (UTRs) of genes, suggesting that their primary mode of action is through regulatory mechanisms that impact gene expression patterns.[1] These regulatory influences can involve epigenetic modifications, such as specific histone marks (e.g., H3K4me1 and H3K27ac), and manifest as various molecular quantitative trait loci (QTLs), including expression QTLs (eQTLs), mRNA splicing QTLs (sQTLs), or histone modification QTLs (hQTLs), with some variants demonstrating colocalization with molecular QTLs in corresponding cell types.[1]

Section titled “Clinical Relevance and Pathophysiological Links”

Variations in basophil percentage, similar to other hematological indices, hold significant clinical implications and are associated with a range of common complex diseases.[1] The broader understanding derived from studies of blood cell traits indicates that their levels can reflect underlying pathophysiological processes, including immune system dysregulation, inflammatory responses, or systemic reactions to stress.[1] Genetic insights into blood cell traits frequently uncover connections to inherited disorders of the hematopoietic system, blood cancers, and various autoimmune or inflammatory conditions, underscoring their systemic consequences.[1]Beyond genetics, it is also recognized that non-genetic factors such as age, sex, menopause status, and even technical aspects of sample handling (e.g., time between venipuncture and analysis) contribute considerably to the observed variance in blood cell indices, emphasizing the multifactorial nature of maintaining hematological homeostasis.[1]

Genome-wide association studies (GWAS) have extensively elucidated the genetic architecture underlying blood cell traits, including basophil percentage of leukocytes.[2] These studies have revealed a detailed atlas of genes and regulatory regions that influence blood cell indices with cell-type-specific effects.[1] Many identified common genetic variants are non-coding, indicating their role in regulatory mechanisms rather than directly altering protein sequences.[1]These regulatory elements likely impact gene expression through mechanisms such as enhancer or promoter activity, thereby governing the molecular programs that control hematopoietic stem cell differentiation and proliferation, which are foundational to basophil development and overall count.[1]Further insights into gene regulation come from colocalization analyses, where genetic variants associated with basophil percentage may also align with molecular quantitative trait loci (QTLs) for gene expression (eQTL), mRNA splicing (sQTL), or histone modifications (hQTL) in relevant cell types.[1]Such colocalization suggests a shared genetic influence on both the basophil percentage and specific molecular events, highlighting critical gene regulatory pathways involving transcription factor binding and chromatin remodeling that dictate basophil lineage commitment and maturation. The precise interplay of these epigenetic marks and genetic variants fine-tunes the production and maintenance of basophils within the leukocyte population.[1]

The determination of basophil percentage within leukocytes is intrinsically linked to intricate intracellular signaling cascades that govern cell proliferation, survival, and differentiation within the hematopoietic system. While specific basophil signaling pathways are complex, the general principles involve receptor activation on hematopoietic progenitor cells, triggering downstream signaling molecules that ultimately regulate transcription factors.[1]These transcription factors orchestrate the expression of genes crucial for basophil lineage commitment, growth, and maturation, ensuring an appropriate balance of cell types.[1]These signaling pathways are subject to tight feedback loops and allosteric control, maintaining cellular homeostasis and responding to physiological demands. Dysregulation in these cascades, such as altered receptor sensitivity or aberrant intracellular signal transduction, can significantly impact basophil production and survival, leading to deviations in their circulating percentage. The dynamic regulation of these processes ensures that basophil numbers are adjusted in response to various internal and external cues, integrating signals from the broader immune system.[1]

The regulation of basophil percentage does not occur in isolation but is part of a highly integrated system involving extensive pathway crosstalk and network interactions across different blood cell lineages. Genetic variants influencing basophil percentage often exhibit pleiotropy, meaning they are associated with the variance of multiple traits.[2] For instance, a lead vQTL located in the HBM gene has been identified as pleiotropic, impacting the variance of several blood cell traits.[2] This suggests that certain genetic loci operate at a higher hierarchical level, influencing shared progenitor cell pathways or common regulatory networks that affect multiple hematopoietic cell types simultaneously.[1]Such systems-level integration highlights how changes in one pathway can have ripple effects across the entire hematopoietic landscape. The emergent properties of this complex network determine the overall composition of leukocytes, including the basophil fraction. Understanding these network interactions is critical for deciphering how genetic predispositions or environmental factors might broadly reshape immune cell profiles rather than affecting a single cell type in isolation.[1]

Dysregulation within the pathways controlling basophil percentage can contribute to the pathogenesis of various complex human diseases. Research indicates shared genetic links between blood cell traits and conditions such as autoimmune, cardiometabolic, and neuropsychiatric disorders.[1]While basophils are generally a small fraction of leukocytes, their altered percentage can reflect underlying immune system imbalances or inflammatory states, potentially playing a role in disease development.[1] In cases of significant pathway dysregulation, compensatory mechanisms may be activated to mitigate extreme phenotypic effects. For example, the magnitude of rare variant effects on phenotype can be influenced by such compensatory pathways, particularly under stress or demand for adaptation in response to injury.[1]Identifying the specific pathways that are dysregulated in disease states offers potential therapeutic targets for modulating basophil numbers or their function to restore immune homeostasis and ameliorate disease progression.[1]

The basophil percentage of leukocytes, a component of the complete blood count, exhibits significant genetic influence, with genome-wide analyses identifying numerous independent variance quantitative trait loci (vQTLs) for this trait.[2]These genetic factors contribute substantially to the observed variability in basophil percentages across individuals, highlighting a complex interplay between genetics and hematological phenotypes. Understanding these genetic determinants is crucial for personalized medicine approaches, as it can help identify individuals with inherent predispositions to higher or lower basophil percentages, thereby informing risk stratification and potentially guiding preventive strategies based on an individual’s unique genetic profile. For instance, studies involving large cohorts, such as a health check-up cohort with 10,000 Korean individuals, have estimated the heritability of basophil percentage, further underscoring its genetic basis and potential as a biomarker.[3]

Basophil percentage is routinely assessed as part of a comprehensive white blood cell differential, providing valuable insights into immune status and inflammatory processes. Its clinical application extends to diagnostic utility in various conditions, although specific diagnostic thresholds often require further research and context. Rigorous quality control measures are essential for accurate basophil percentage determination, as technical factors like the time elapsed between venipuncture and full blood count analysis, instrument calibration, and non-genetic biological variations such as age, sex, and menopause status can significantly influence results.[1] Such careful adjustments for covariates, including age, sex, BMI, smoking status, and alcohol consumption, are critical for reliable data in large-scale genetic studies and for improving the precision of monitoring strategies in patient care.[2]

Investigating Associations with Complex Diseases

Section titled “Investigating Associations with Complex Diseases”

The basophil percentage of leukocytes has been included in extensive investigations exploring causal associations with a range of common complex diseases, utilizing advanced methodologies like multivariable Mendelian randomization analysis.[1]These studies systematically assess the potential links between various blood cell indices and conditions such as autoimmune diseases (e.g., asthma, inflammatory bowel disease), cardiometabolic disorders (e.g., coronary heart disease, type 2 diabetes), and neuropsychiatric conditions (e.g., schizophrenia, major depressive disorder).[1]

Frequently Asked Questions About Basophil Percentage Of Leukocytes

Section titled “Frequently Asked Questions About Basophil Percentage Of Leukocytes”

These questions address the most important and specific aspects of basophil percentage of leukocytes based on current genetic research.


1. My family has lots of allergies; does that mean my basophils are naturally higher?

Section titled “1. My family has lots of allergies; does that mean my basophils are naturally higher?”

Yes, there’s a good chance. Your basophil percentage is significantly influenced by genetic factors passed down in families, which can make you more prone to allergic reactions. These genetic influences can affect both your typical basophil levels and how much they vary.

Yes, it’s possible. Severe stress reactions are known to be associated with lower basophil levels, a condition called basopenia. Your body’s response to stress can directly impact your immune cell counts, including basophils.

It can. Genetic factors influencing basophil percentage can vary significantly across different ethnic populations. What’s considered typical or a risk factor in one group might be different in another, highlighting the need for diverse research.

Potentially, yes. Genetic studies have identified specific genetic variations that influence not only the average basophil levels but also their variability within individuals. Understanding these genetic factors could offer insights into why your levels fluctuate.

Yes, they can. Variations in blood cell traits, including basophil percentage, have been linked to susceptibility to common complex diseases like autoimmune conditions, heart issues, and even some brain-related disorders. It’s an indicator of your overall immune system status.

6. My doctor said my basophils are high, but I feel totally fine. Why?

Section titled “6. My doctor said my basophils are high, but I feel totally fine. Why?”

It’s possible. Elevated basophil levels (basophilia) can sometimes signal underlying conditions like allergic reactions or chronic inflammation that you might not be fully aware of yet. Genetic factors also play a role in determining your baseline levels, which can naturally be on the higher side for some individuals.

7. If I start eating super healthy, can I significantly change my basophil percentage?

Section titled “7. If I start eating super healthy, can I significantly change my basophil percentage?”

While a healthy lifestyle is always beneficial, your basophil percentage is a tightly controlled biological trait with significant genetic influences. Environmental factors certainly play a role, but genetic predispositions contribute significantly to your baseline levels and how much they can shift.

Yes, it does. Non-genetic factors like age are known to explain a substantial portion of the variation in basophil percentage. Clinicians consider age, along with other factors like sex, when interpreting your blood test results.

9. If my parents have certain health issues, could my basophils be connected to that?

Section titled “9. If my parents have certain health issues, could my basophils be connected to that?”

Yes, there’s a strong possibility. Genetic factors are known to influence basophil levels, and these same genetic influences can be linked to susceptibility to various common diseases, including autoimmune, cardiometabolic, and neuropsychiatric conditions that might run in families.

10. Why do some people seem to have more severe allergic reactions than others?

Section titled “10. Why do some people seem to have more severe allergic reactions than others?”

Genetic factors play a significant role in this. Basophils are key mediators of allergic reactions, and the genetic architecture influencing basophil production and function can vary between individuals, leading to differences in immune responses and the severity of allergies.


This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.

Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.

[1] Astle WJ, et al. “The Allelic Landscape of Human Blood Cell Trait Variation and Links to Common Complex Disease.”Cell, 2016.

[2] Xiang R, et al. “Genome-wide analyses of variance in blood cell phenotypes provide new insights into complex trait biology and prediction.” Nat Commun, 2024.

[3] Choe, E. K., et al. “Leveraging deep phenotyping from health check-up cohort with 10,000 Korean individuals for phenome-wide association study of 136 traits.” Sci Rep, vol. 12, no. 1, 2022, p. 1930.