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CD4‐positive cells from patients with IgA nephropathy demonstrate increased mRNA of cytokines that induce the IgA switch and differentiation
Author(s) -
Lai Kar Neng,
Lui Siu Fai,
Li Philip K. T.,
Ho Rainbow T. H.,
Leung Joseph C. K.,
Chui Y. L.,
Lim P. L.
Publication year - 1994
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711740104
Subject(s) - isotype , nephropathy , cytokine , immunology , biology , glomerulonephritis , immunoglobulin class switching , pathogenesis , messenger rna , transforming growth factor , antibody , endocrinology , gene , b cell , kidney , monoclonal antibody , diabetes mellitus , biochemistry
IgA nephropathy (IgAN) is characterized by raised serum IgA 1 deposits. We have previously shown increased T‐cell activation in IgAN. Recently, transforming growth factor‐β (TGF‐β) has been shown to induce IgA isotype switch at a clonal level and interleukin 5 (IL5) promotes differentiation into IgA‐bearing B cells. In the present study we have examined the TGF‐β and IL5 mRNA expression by mitogen‐activated CD4‐positive T cells from patients with IgAN ( n =25), patients with other primary nephritides (CGN) ( n =24), and healthy control subjects ( n =25). The cytokine genes were analysed by reverse transcription (RT)‐polymerase chain reaction (PCR) and were semi‐quantitated by normalizing the differences occurring during RT and PCR using a housekeeping gene, β‐actin. CD4‐positive T cells from IgA nephritic patients expressed a higher level of IL5 mRNA than healthy controls ( P <0.01) and patients with CGN ( P <0.005). CD4‐positive T cells from IgA nephritic patients expressed a higher level of TGF‐β mRNA than healthy controls ( P <0.01) but no difference was demonstrated on comparison with CGN patients. Elevated TGF‐β mRNA expression in patients with CGN probably reflects its other important function as a (sclerogenic) factor involved in the glomerulosclerosis found in these nephritides. Our data suggest that there is increased expression of cytokine genes which induce the IgA isotype switch and differentiation; these immunological abnormalities may be important in the pathogenesis of IgAN.