4 Western blot analysis of chondrocyte extract. chondrocyte membrane by integrins and its presence in chondrocyte extract is not surprising. Antibody response to COMP raises a question whether the observed changes in tracheal cartilage and epithelium represent anti-COMP reaction or were caused by some other, no specified factors. COMP is used as the marker of osteoarthritis progression, but its role in polychondritis, cartilage pathology involving i.a. tracheal cartilage resorption remains unknown. Thus, our observations may serve as the starting point for future studies in this direction. Keywords: chondrocyte antigen, cartilage oligomeric matrix protein (COMP), transmembrane p24 trafficking protein 10 (TMP21) Introduction Surface chondrocyte molecules of cartilage may serve as an example of sequestered antigens due to the presence of cartilage matrix preventing their contact with immune system [1-3]. Cartilage matrix contains the collagen network composed of types II, IX, and XI collagens, the large aggregating proteoglycan C aggrecan, and a large number of other molecules such as Atglistatin several small proteoglycans: biglycan, decorin, fibromodulin, matrilins, and cartilage oligomeric matrix protein (COMP) [4, 5]. It is well established that collagen type II [6] and proteoglycans are able to stimulate immune response [7], but the antigenicity of chondrocytes and particularly the presence C or absence C of hypothetical tissue specific antigens remains as the no resolved puzzles of chondrocytes biology. Early work showed that isolated allogeneic chondrocytes after transplantation produce cartilage but also evoke the host immunization leading to rejection of new-formed tissue [8]. Demonstration of class I MHC expression by chondrocytes followed [9-12] subsequent publications indicated that chondrocytes are able to present antigens within MHC class II context [13, 14]. In the more recent work, both human articular chondrocytes originating from patients who suffer from osteoarthritis (OA) and from healthy donors were shown to express both class I and class Atglistatin II MHC antigens [15]. In another study, however, authors found that cultured human OA Atglistatin chondrocytes expressed MHC class I but not MHC class II or positive co-stimulatory molecules, and failed to evoke both MHC class I and II mismatch allogeneic lymphocyte responses [16, 17]. Several authors suggested also that chondrocytes express chondrocyte-specific differentiation antigen. Langer [18] have found that rats injected with syngeneic chondrocytes or cartilage shavings developed autoreactivity as assayed by leukocyte migration test. This result, according to the authors, indicated existence of a specific chondrocyte differentiation antigen. This conclusion was supported by studies demonstrating stimulation of proliferative response of rat lymphocytes in mixed lymphocyte-chondrocyte cultures not only by allogeneic but also by syngeneic chondrocytes [19, 20]. The last KI67 antibody observation was confirmed with rabbit [14], human, bovine [21] and rat chondrocytes [11, 22]. To obtain antibodies against chondrocyte-specific differentiation antigen rat chondrocytes were injected into rabbits. Chondrocytes reconstructed cartilage which within two weeks deteriorated, but Atglistatin the sensitized rabbits sera contained high titter of antichondrocyte cytotoxic antibodies which detected antigen with Mr of ~74 and ~23 kDa in chondrocyte lysates. Only the latter remained after reduction in 2-mercaptoethanol. Neither antigen could be detected by this serum in lysates of fibroblasts, endotheliocytes, or thymocytes. Thus, it appeared that the antibodies of this serum reacted with chondrocyte-associated antigen (CAA), but the nature of the antigen remained unknown [23]. Since it is well established that chondrocytes grown in monolayer culture gradually decrease expression of typical matrix molecules such as collagen type II and aggrecan [24, 25], it seemed interesting to establish whether in such cultures expression of chondrocyte-specific differentiation antigen, or, as.
