Immunoglobulins in carcinoma cervix.
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Biomedical subjects
Publications and source records attributed to K Balakrishnan.
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The immune system has evolved in the human being as an elaborate mechanism to distinguish itself from all else that is not self. This process serves in the defence against invaders. The cells of the immune system learn to tolerate all tissues, cells and proteins of the body. Failure to control the state of tolerance results in autoimmunity. The understanding of the role of T-cell receptors (TCR), the Major Histocompatibility Complex (MHC), adhesion molecules and growth factors in antigen recognition has lead to the exploration of various means to modulate the immune response. Safety measures exist to prevent the immune system from attacking its host. The antigen has to be recognized by the T-cell. This involves the TCR and the MHC. In addition it must receive a second signal to become activated. The second signal involves a protein such as B7 binding with CD28. Certain specialized cells, macrophages, dendritic cells and activated B-cells can deliver this second signal for activation; receipt of only one signal can prevent activation. The elucidation of the role of cell-to-cell interactions, the adhesion molecules involved and the accessory growth factors provides modalities for selectively modifying the immune response. This would be of great relevance in autoimmunity and transplantation.
In a study of 32 white patients with systemic lupus erythematosus from 28 families, 60 unique chromosome 6 haplotypes were defined. The MHC extended haplotype HLA-B8, -DR3, SC01, GL02 was strongly disease-associated (0.09 patients, 0.02 controls, RR = 4.5, C.I. = 1.6-12.4, P less than 0.05), while the corresponding haplotype with the GL01 specificity was not increased in frequency (0.05 in both patients and controls). In the present data, the increase in the haplotype bearing GL02 accounted entirely for the association between HLA-DR3 and SLE. Furthermore, the phenotype of complete C4A deficiency was also strongly disease-associated (patients 0.14, controls 0.02, RR = 8.5, C.I. = 1.8-37.0, P less than 0.05). The only other MHC association in these patients was an increased occurrence of the HLA-B17, -DR7, SC61 haplotype (patients 0.07, controls 0.01, RR = 6.0, C.I. = 1.8-20.6, P corr. less than 0.05). The relationship between MHC markers and autoimmune disease appears to be a result of an association with MHC extended haplotypes and complete complement component deficiencies rather than with individual alleles. It is important that future studies include family members so that such haplotypes can be defined.
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