HLA-Cw*0602 associates with a twofold higher prevalence of positive streptococcal throat swab at the onset of psoriasis: a case control study.
BACKGROUND
The influence of streptococcal infections in the pathogenesis of psoriasis is not yet understood. In vitro data suggest that streptococcal factors influence T-cell function in psoriasis in a HLA-dependent manner, but studies designed to measure the HLA-C/Streptococci interaction are lacking. In the present study, we hypothesized that there is a statistical interaction between the result of streptococcal throat cultures and the presence of the HLA-Cw*0602 allele in psoriasis patients.


METHODS
We performed a case control study using the "Stockholm Psoriasis Cohort" consisting of patients consecutively recruited within 12 months of disease onset (Plaque psoriasis = 439, Guttate psoriasis = 143), matched to healthy controls (n = 454) randomly chosen from the Swedish Population Registry. All individuals underwent physical examination including throat swabs and DNA isolation for HLA-Cw*0602 genotyping. The prevalence of positive streptococcal throat swabs and HLA-Cw*0602 was compared between patients and controls and expressed as odds ratios with 95% confidence intervals. Associations were evaluated separately for guttate and plaque psoriasis by Fisher's exact test.


RESULTS
Regardless of disease phenotype, the prevalence of positive streptococcal throat swabs in HLA-Cw*0602 positive patients was twice the prevalence among HLA-Cw*0602 negative patients (OR = 5.8 C.I. = 3.57-9.67, p < 0.001), while no difference was observed among Cw*0602 positive versus negative controls. The corresponding odds ratios for the guttate and plaque psoriasis phenotypes were 3.5 (CI = 1.5-8.7, p = 0.01) and 2.3 (CI = 1.0-5.1, p = 0.02) respectively.


CONCLUSIONS
These findings suggest that among HLA-Cw*0602 positive psoriasis patients, streptococci may contribute to the onset or exacerbation of the inflammatory process independent of the disease phenotype. However, studies on the functional interaction between HLA-C and streptococcal factors are needed.
Mallbris
Lotus
L
Dermatology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. lotus.mallbris@ki.se
Wolk
Katarina
K
Sánchez
Fabio
F
Ståhle
Mona
M
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D005838:Genotype; D015236:HLA-C Antigens / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010612:Pharyngitis / Q000453:epidemiology / Q000235:genetics / Q000382:microbiology; D015995:Prevalence; D011565:Psoriasis / Q000453:epidemiology* / Q000235:genetics*; D012042:Registries; D013290:Streptococcal Infections / Q000453:epidemiology* / Q000235:genetics*; D055815:Young Adult
D015236:HLA-C Antigens; C491620:HLA-C*06:02 antigen