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"Our study provides evidence that HLA alleles are involved in antibody responsiveness or non-responsiveness to Bb infection. A low frequency of HLA-DR7 alleles
and HLA-DR6 alleles and a high frequency of HLA-DR1 alleles may contribute to non-responsiveness of antibody production in LD patients. Thus, genetic
predisposition may be a critical factorFactor ix complex in the regulation of the host immune response and the diagnosis and prognosis of Lyme disease.”
source:
2001 Contribution of HLA alleles in the regulation of antibody production in Lyme disease. Front Biosci, 6:B10-B16
A small subset of patients infected with Borrelia burgdorferi (Bb) does not produce Bb specific antibody. Our research provides additional evidence of a genetic predisposition for seronegativity in some individuals with Lyme disease. Because humanHcg in urine Hiv infection Human bites Human papillomavirus vaccineleukocyteLeukocyte alkaline phosphataseantigenCea Histocompatibility antigen test Hla-b27 antigen Psa (HLA) class II, a heterodimeric glycoprotein, plays an essentialEssential balance Essential hypertension Essential tremor role in the regulation of antibody production, we investigated the difference in HLA genes between seropositive and seronegative patients with Lyme disease (LD). Our results show that HLA-DR7 was associated with anti-Bb antibody production. Nine out of the 22 seropositive LD patients (40.9%) had HLA-DRB1*0701, *0703, *0704 (HLA-DR7); only 1 out of the 18 seronegative LD patients (5.6%) had HLA-DR7 (odds ratio (OR)=11.8, P=0.0126). HLA-DRB1*01021 and HLA-DRB1*0101, *0104, *0105 (HLA-DR1) contributed negatively to anti-Bb antibody production. Seven of 18 seronegative LD patients had HLA-DR1, only 1 of 22 seropositive LD patients had HLA-DR1 (38.9% vs. 4.5%, OR=13.4, P=0.0138). These results suggest that the presence and or lack of production of specific antibody to Bb infection may be associated with particular HLA specificities of the Class II.
A small subset of patients infected with Borrelia burgdorferi (Bb) does not produce Bb specific antibody. Our research provides additional evidence of a genetic predisposition for seronegativity in some individuals with Lyme disease. Because human leukocyte antigen (HLA) class II, a heterodimeric glycoprotein, plays an essential role in the regulation of antibody production, we investigated the difference in HLA genes between seropositive and seronegative patients with Lyme disease (LD). Our results show that HLA-DR7 was associated with anti-Bb antibody production. Nine out of the 22 seropositive LD patients (40.9%) had HLA-DRB1*0701, *0703, *0704 (HLA-DR7); only 1 out of the 18 seronegative LD patients (5.6%) had HLA-DR7 (odds ratio (OR)=11.8, P=0.0126). HLA-DRB1*01021 and HLA-DRB1*0101, *0104, *0105 (HLA-DR1) contributed negatively to anti-Bb antibody production. Seven of 18 seronegative LD patients had HLA-DR1, only 1 of 22 seropositive LD patients had HLA-DR1 (38.9% vs. 4.5%, OR=13.4, P=0.0138). These results suggest that the presence and or lack of production of specific antibody to Bb infection may be associated with particular HLA specificities of the Class II.