106 patients with axial spondylarthritis (SpA), 98 patients with knee joints osteoarthritis (OA) and 136 patients with rheumatoid arthritis (RA) are included in research. At all patients are investigated polymorphism of cytokines genes TNFА (rs361525, rs1800629 rs1800630), IL1β (rs1143627), IL4 (rs2243250), IL6 (rs1800795), IL10 (rs1800872, rs1800872), IL17(rs2275913, rs763780), vascular endothelial growth factor gene VEGF (rs3025039, rs699947), matrix metalloproteinases genes MMP2 (rs2438650), MMP3 (rs3025058), MMP9 (rs3918242). Genetic attributes which meet various frequency among patients with RA and which are never revealed in group of SpA or OA patients, and alternative attributes which in one case are not revealed among patients with RA, and frequently come to light among patients with SpA or OA are allocated. These attributes alternativeness allows to use them with a high degree of reliability as additional laboratory criteria of the differential diagnosis at early stages of joints diseases development.
The greatest risk of the development of joints pathology is connected with HLA DRB 1*01, HLA DRB 1*04. However, not all HLA DRB 1*01, HLA DRB 1*04 positive individuals suffer this pathology. The specific interactions between hsp70 and HLA DRB 1 can promote the pathological process, because hsp70 can function as molecular chaperone and participate in processing and presentation of antigenic peptides. We have considered an influence of HSP70-2 and HSP70-HOM genes polymorphism in the coding regions and their association with HLA DRB1 in patients with rheumatoid arthritis. An increased risk of RA development was observed in patients with HSP70-2*B/B/ HSP70-HOM*A/A and HSP70-2 *B/B/ HSP70-HOM* B/B/ phenotypes. The risk of RA development in HLA-DRBl*01/*04 positive groups increased in patients with HSP70-2* B/B/ HSP70-HOM*A/A phenotype. The obtained data reveal that gene allelic variants of processing, along with gene allelic variants of presentation, may indicate the efficiency of the immune response and, probably, influence the development of autoimmune processes. (Med. Immunol., 2001, vol. 3, N 4, pp 551-556)