Association between Human Leukocyte Antigen Class II Alleles and Genotype ofBorrelia burgdorferiin Patients with Early Lyme Disease

Abstract

The DRB1*0101 allele and the DRB1*0101-DQB1*0501 haplotype may be relevant to the development of infection with strains from the least invasive genotypes of B. burgdorferi.

T‐Cell Epitope Mapping of the Borrelia garinii Outer Surface Protein A in Lyme Neuroborreliosis

“…A number of peptides (OspA [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] [21,20]. Patients with treatment resistant Lyme arthritis have also been associated with the HLA-DR4, DR2 [27] and DRB1 [28,29], further supporting the involvement of an autoantigen in these patients.…”

“…Patients with treatment resistant Lyme arthritis have also been associated with the HLA‐DR4, DR2 [27] and DRB1 [28, 29], further supporting the involvement of an autoantigen in these patients. In patients with early Lyme disease (erythema migrans), associations have been demonstrated between HLA DR haplotypes and genotypes of B. burgdorferi s.s. [30]. Although HLA associations in neuroborreliosis have been suggested, no firm HLA‐associations have been clearly demonstrated [31–36].…”

“…In early experiments a few peptides were more able to stimulate lymphocytes from neuroborreliosis patients, namely no 1 (OspA [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] Blood and CSF cells from patients and controls were stimulated with 29 different high-purity overlapping peptides from OspA ( Table 3). The peptides had a clearcut IFN-c stimulating capacity in lymphocytes from some patients, whereas cells from other patients hardly responded to any of the peptides.…”

Increased prevalence of Borrelia burgdorferi infections in Bernese Mountain Dogs: a possible breed predisposition

“…It is well established that Borrelia organisms evade the immune system in different ways and host factors become more important the less pathogen the responsible organisms are [14,15]. In human patients with Lyme disease-associated erythema migrans, the carriage rate of leukocyte class II alleles DRB1*0101 and DRB1*0101-DQB1*0501 was higher in patients with the least pathogen B. burgdorferi genotype [15].…”

“…In human patients with Lyme disease-associated erythema migrans, the carriage rate of leukocyte class II alleles DRB1*0101 and DRB1*0101-DQB1*0501 was higher in patients with the least pathogen B. burgdorferi genotype [15]. The immunologic event causing this association was not known but as DRB1 alleles are located close to certain major histocompatibility complex-encoded complement genes, it was speculated that variants of these complement genes might be in linkage disequilibrium with the DRB1 alleles [15,16]. The innate immune response plays an important role in the early response of Borrelia [17] but it also plays a role in the development of certain glomerular diseases.…”