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In this study, we assessed the LFA-1 (CD18/CD11a) and CR3 (CD18/CD11b) expression on peripheral polymorphonuclear leukocytes (PB-PMN) and crevicular fluid polymorphonuclear leukocytes (CF-PMN), by subjects with a healthy periodontium (n= 7), gingivitis (n= 8), early-onset periodontitis (n= 17) and adult periodontitis (n= 8). Using flow cytometry analysis, the %s of CD18, CD11a and CD11b positive cells and the absolute numbers of fluorescent molecules were determined. No significant difference could be found among the 4 groups, for these 2 kinds of parameters, in PB-PMN or CF-PMN. However, a great difference could be noted between the results obtained from PB-PMN and those obtained from CF-PMN. The %s of positive CF-PMN were significantly lower than those of PB-PMN for the 3 sub-units (p ͎ 0.001). The levels of CD18 and CD11b expressed by CF-PMN were higher than those expressed by PB-PMN and the difference was significant for CD11b (p < 0.001). On the contrary, the level of CD11a expressed on CF-PMN was significantly lower than that expressed by PB-PMN (p< 0.001). Hence, our current results show that early-onset periodontitis PMN can be quite normal and this fact is not surprising insofar as, in our study, these cells were perfectly functional and all the subjects were in good health. We concluded that the analysis of the leukocyte adhesion receptors expression on PB-PMN does not appear useful for helping to establish a differential diagnosis between the different forms of periodontitis. However, the pattern of expression study on CF-PMN may permit a better comprehension of the local phenomena which are implicated in the defence of the periodontal tissues against oral micro-organisms. [ABSTRACT FROM AUTHOR]

The HLA-DM molecule catalyses the CLIP/antigen peptide exchange in the classical class II peptide-binding groove. As such, DM is an antigen presentation regulator and may be linked to autoimmune diseases. Using PCR derived methods, a relationship was revealed between DM gene polymorphism and IDDM, in a Corsican population. The DMA*0101 allele was observed to confer a significant predisposition to this autoimmune disease while the DMA*0102 allele protected significantly. Experiments examining polymorphism of the HLA-DRB1 gene established that these relationships are not a consequence of linkage disequilibrium with HLA-DRB1 alleles implicated in this pathology. The study of the DMA gene could therefore be an additional tool for early IDDM diagnosis in the Corsican population. [ABSTRACT FROM AUTHOR]

The HLA-DMA gene, along with the HLA-DMB gene, encodes the not classical class II molecule. This molecule catalyzes the class-II-associated invariant-chain peptide (CLIP)-antigen peptide exchange in classical class II molecule peptide-binding groove. As such, the DM heterodimer is an antigen presentation regulator and may be linked to immune system deficiencies such as those observed in autoimmune diseases. The study of DMA gene polymorphism seems be a reasonable approach to provide an answer to this question. Thanks to PCR-derived methods, the relationship between DMA gene polymorphism and rheumatoid arthritis (RA) was demonstrated in the present study. The DMA*0101 allele was observed to confer a significant predisposition to RA while the DMA*0102 allele significantly protected from this disease. Polymorphism experiments with the HLA-DRB1 gene revealed that this relationship between DMA polymorphism and RA is not a consequence of a linkage disequilibrium with the HLA-DRB1 alleles implicated in this pathology. The study of the DMA gene could therefore prove to be very useful in the early diagnosis of RA., (Copyright 1999 S. Karger AG, Basel)

The cerebrospinal fluid (CSF) represents an important source of T lymphocytes that could be involved in the inflammatory response occurring in the central nervous system in multiple sclerosis (MS). In order to investigate whether the Vbeta gene usage of CSF T lymphocytes is restricted, we analyzed the TCR Vbeta expression in twelve CSF expanded by in vitro culture compared to the paired in vitro-stimulated peripheral blood T lymphocytes. The overexpression of one or two Vbeta genes was demonstrated in ten CSF, but the type of Vbeta over expressed varied from one patient to another. For one patient, the Vbeta repertoire was also investigated by single cell cloning. High frequency of BV6S7-expressing T cell clones was observed in the CSF while no BV6S7 clone was derived from the peripheral blood T lymphocytes suggesting that these cells could be involved in the immunopathological process in the central nervous system (CNS). The cytokine patterns of the T cell clones derived from the CSF- and peripheral blood-T lymphocytes of this patient were determined. The CSF T cell clones produced higher levels of cytokines than the peripheral blood T cell clones. The high frequency of IL-4-producing-T cell clones observed in CSF demonstrate that T cells which could downregulate the inflammatory process are present in the CNS.