What you carry at this position in your DNA and what research says about it.
Psoriasis Risk: 8/10 evidence, 9 publications.
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Sample genotype (not yours): C/C
Typical Risk of Psoriasis and Psoriatic Arthritis
Carrying two copies of the common C allele is associated with a typical baseline risk for developing psoriasis and its related joint complications. This genotype does not carry the highly influential HLA-Cw*06:02 risk variant.
What this genotype means: Typical baseline risk of psoriasis; Typical baseline risk of psoriatic arthritis.
Sample genotype (not yours): C/T
Increased Risk of Psoriasis and Psoriatic Arthritis
Carrying one copy of the T allele significantly elevates the risk of developing psoriasis and psoriatic arthritis. However, this genetic profile is also associated with a more favorable response to certain biologic treatments.
What this genotype means: Elevated risk of psoriasis; Elevated risk of psoriatic arthritis; Better response to anti-TNF therapies.
Sample genotype (not yours): T/T
Highly Increased Risk of Psoriasis and Psoriatic Arthritis
Carrying two copies of the T allele is associated with a highly elevated risk of developing psoriasis, often with an earlier age of onset. Fortunately, this profile is linked to a significantly better response to anti-TNF biologic therapies.
What this genotype means: Highly elevated risk of psoriasis; Highly elevated risk of psoriatic arthritis; Significantly better response to anti-TNF therapies.
Gene function and biological role
Gene Function: Human leukocyte antigen C belongs to the major histocompatibility complex class I family, playing a critical role in the immune system's ability to distinguish self from non-self. This gene encodes a cell surface glycoprotein that presents intracellular peptides to cytotoxic T cells and interacts with natural killer cell receptors. Variations within this region are heavily implicated in autoimmune and inflammatory conditions due to altered antigen presentation. In particular, certain alleles are strongly associated with susceptibility to chronic skin conditions like psoriasis [1]. The gene is also a key determinant in transplant compatibility and host defense against viral infections.
Variant Impact: This intergenic single nucleotide polymorphism is located on chromosome 6 near the HLA-C gene. The genetic variation serves as a highly accurate proxy marker for the HLA-Cw*06:02 allele, which is the primary genetic risk factor for psoriasis [1]. The presence of the variant allele alters immune system recognition, leading to autoimmune targeting of skin cells [2]. This specific change is also linked to the development of joint inflammation in psoriatic arthritis [3].
Key Insight: The same genetic variant that increases the risk of developing psoriasis also makes a person significantly more responsive to advanced anti-TNF biologic treatments.
Location: HLA-C. Chromosome 6 · 6p21.33 · 31.3 Mb
Estimated prevalence by population
Global 76.8%; European 74.8%; African 80.3%; East Asian 89.5%; South Asian 69.8%; Americas 79.2%; Ashkenazi 47.7%; Finnish 80.9%; Middle Eastern 58.6%; Amish 60.8%.
Estimated CC genotype frequency.
Global 21.6%; European 23.4%; African 18.6%; East Asian 10.2%; South Asian 27.5%; Americas 19.5%; Ashkenazi 42.8%; Finnish 18.0%; Middle Eastern 35.9%; Amish 34.4%.
Estimated CT genotype frequency.
Global 1.7%; European 1.8%; African 1.1%; East Asian 0.3%; South Asian 2.7%; Americas 1.2%; Ashkenazi 9.6%; Finnish 1.0%; Middle Eastern 5.5%; Amish 4.9%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Organ Systems
Skin & Hair Conditions
Psoriasis. Evidence: 8/10. Source: PMID 19169254. Typical Risk.
Age of Psoriasis Onset. Evidence: 8/10. Source: PMID 19680446. Typical Onset.
Immunity & Inflammation
Autoimmune Diseases
Psoriatic Arthritis. Evidence: 6/10. Source: PMID 26626624. Typical Risk.
Pharmacogenomics
Immunosuppressant & Biologic Response
Anti-TNF Drug Response. Evidence: 5/10. Source: PMID 27670765. Typical Response.
Showing effects for C/T genotype
Psoriasis. Evidence: 8/10. Source: PMID 19169254. ~2.6x Increased Risk.
Age of Psoriasis Onset. Evidence: 8/10. Source: PMID 19680446. Earlier Onset.
Psoriatic Arthritis. Evidence: 6/10. Source: PMID 26626624. Increased Risk.
Anti-TNF Drug Response. Evidence: 5/10. Source: PMID 27670765. Stronger Response.
Showing effects for T/T genotype
Psoriasis. Evidence: 8/10. Source: PMID 19169254. Highly Increased Risk.
Psoriatic Arthritis. Evidence: 6/10. Source: PMID 26626624. Highly Increased Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Baseline genetic risk for autoimmune skin disorders is maintained by this genotype. The absence of the T allele means the immune system is less likely to mistakenly target healthy skin cells through the specific HLA-Cw*06:02 pathway [1]. Studies show that individuals with this genetic profile have a significantly lower incidence of plaque psoriasis compared to T allele carriers [2]. Joint health is also favored, as the risk for psoriatic arthritis remains at the typical population level [3]. If psoriasis does develop due to other factors, the age of onset is typically later. Response to standard anti-TNF therapies is typical, as this genotype lacks the specific variant associated with altered drug efficacy [4]. Overall, this profile represents the most common genetic baseline across global populations.
Typical baseline risk of psoriasis; Typical baseline risk of psoriatic arthritis.
Sample genotype: CT (Heterozygous)
Elevated susceptibility to chronic inflammatory skin plaques is a primary feature of this genetic profile. Having one copy of the T allele introduces the HLA-Cw*06:02 risk factor, which triggers autoimmune activity against skin cells [1]. Research indicates this variant is the strongest genetic predictor for early-onset psoriasis [2]. Joint inflammation is also more common, raising the likelihood of developing psoriatic arthritis over time [3]. Despite these risks, carriers often experience a better therapeutic response to tumor necrosis factor (TNF) inhibitors [4]. This enhanced drug response can make certain biologic therapies highly effective if treatment becomes necessary. Managing environmental triggers like stress and skin injuries remains important for maintaining skin health.
Elevated risk of psoriasis; Elevated risk of psoriatic arthritis; Better response to anti-TNF therapies.
Sample genotype: TT (Homozygous)
Strong genetic predisposition to autoimmune skin and joint conditions characterizes this homozygous profile. Carrying two copies of the T allele strongly correlates with the presence of the HLA-Cw*06:02 antigen, a major driver of skin autoimmunity [1]. This genetic setup frequently leads to an earlier onset of plaque psoriasis, often appearing before age forty [2]. The risk of developing painful joint inflammation via psoriatic arthritis is also substantially elevated [3]. On the positive side, clinical studies show that individuals with this genotype respond exceptionally well to anti-TNF biologic medications [4]. This high sensitivity to treatment offers a reliable therapeutic pathway if moderate-to-severe symptoms occur. Proactive skin care and avoiding known inflammatory triggers are highly recommended strategies.
Highly elevated risk of psoriasis; Highly elevated risk of psoriatic arthritis; Significantly better response to anti-TNF therapies.
Variants with shared genetic architecture
rs10484554 · HLA-C Gene · Chr 6 · Psoriasis Risk
rs9264942 · HLA-C Gene · Chr 6 · Viral Control and Crohn's
rs33980500 · TRAF3IP2 Gene · Chr 6 · Psoriatic Arthritis Risk
Multiple Loci within the major histocompatibility complex confer risk of psoriasis.
Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways.
Content updated August 2026.
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