Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Class II major histocompatibility antigens (Ia) play a major role in regulating T-B cell interactions; therefore, regulation of the amount of Ia on B cells may be an important point of control in the immune response. Mitogens in human and murine systems have been reported to increase Ia expression on B cells, and in the mouse the lymphokine BSF-1 (IL-4) markedly enhances Ia expression. This report describes studies of lymphokine and mitogen regulation of class II expression on rat B cells. Mitogens known to activate resting B cells, such as DxS/LPS, anti-IgM, STM, and Con A, induced increases in Ia expression. Highly purified murine IL-4 was found to have no Ia-enhancing activity on rat B cells, although the same preparation increased Ia expression eightfold on murine B cells. This confirms other recent reports that IL-4 is a species-specific lymphokine and will not cross even narrow phylogenetic barriers. Rat B cells were not refractory to lymphokine-induced enhancement of Ia expression, since lymphokine(s) contained in a Con A-induced supernatant enhanced Ia expression. Furthermore, murine IL-5-containing B151-CFS was able to markedly increase Ia expression on resting rat and mouse B cells. This activity was not lost after heat inactivation of B151-TRF2, indicating that B151-TRF1 (IL-5-like activity) was probably responsible for the increase in Ia expression. These results suggest Ia expression on rat B cells, like human and murine B cells, is an early activation event which is regulated by signals which act on resting B cells. Furthermore, while IL-4 is important in Ia regulation, it is not the only lymphokine involved, since the IL-4-free, B151-K12 supernatant was able to enhance Ia expression on resting rat and mouse B cells.
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PMID:Lymphokine regulation of surface Ia expression on rat B cells. 325 20

We demonstrated previously that cellfree supernatant of the B151K12 T cell hybridoma (B151-CFS) contained T cell-replacing factor (here in after referred to as B151-TRF1) capable of inducing growth and differentiation of antigen-activated B cells into antigen-specific plaque-forming cells (PFC). In the present study, we have identified in B151-CFS another unique lymphokine activity (referred to as B151-TRF2), which induces polyclonal differentiation of unstimulated B cells into IgM-secreting cells without concomitant stimulation of antigen, mitogen, or anti-Ig antibody. The B151-TRF2 activity induced polyclonal IgM PFC responses via the action on surface Ig-positive small resting B cells from normal unprimed mice. This activation was effective across an H-2 barrier, and apparently independent of the presence of T cells and accessory cells. Interestingly, the B151-TRF2 activity notably stimulated B cells of neonatal and mutant DBA/2Ha mice, which are nonresponders to B151-TRF1, whereas it failed to activate the xid B cells from CBA/N mice. To substantiate that B151-TRF1 and B151-TRF2 activities are mediated by mutually distinguishable molecules, an absorption experiment of B151-CFS was performed by utilizing DBA/2Ha B cells which are lacking in B151-TRF1 receptor. It was found that DBA/2Ha B cells could absorb B151-TRF2 activity but not B151-TRF1 activity. In contrast, murine chronic B cell leukemia BCL1 cells, which were shown to differentiate into IgM-secreting cells by stimulation with B151-CFS, selectively removed B151-TRF1 activity but not B151-TRF2 activity. Furthermore, biochemical analysis revealed that the B151-TRF2 was a heat (56 degrees C for 30 min)-sensitive protein with an apparent m.w. of 30,000 by gel filtration, whereas B151-TRF1 was a heat-resistant glycoprotein with m.w. of 50,000. In addition, it was shown that prostaglandin E2 selectively inhibited B151-TRF2-mediated B cell responses. These results demonstrate clearly that B151-TRF1 and B151-TRF2 are distinct B cell differentiation factors involved in the different activation pathways of distinct B cell subpopulations. The immunologic implication of B151-TRF2 activity in B cell differentiation is discussed in comparison with other lymphokines so far reported to activate small resting B cells.
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PMID:Identification of two distinct factors, B151-TRF1 and B151-TRF2, inducing differentiation of activated B cells and small resting B cells into antibody-producing cells. 351 74