1994年 · 第10卷第04期

Lymphocyte subsets infiltrated in interstitium of IgA-N were analysed

The numbers of T, B lymphocytes infiltrated in interstium were varied with histologicl lesions, immuuopathologic types and clinical manifestations. The more severe of histologic lesions, the higher the numbers of T, B lymphocyte subsets, the lower of the ratios.

It is suggested that lymphocyte subsets may be regards as one of marks to classified IgA-N, and also it may be predicated the severity of histological lesions.

This study was designed to investigate whether there is an antagonistic effect of MsC-derived IL-1 and PGE2 on MsC proliferation. Experimental results showed that: (1) MsC stimulated by LPS could produce IL-1; (2) MsC stimulated by MsC-derived IL-1 could release PGE2; (3) exogenous PGE2 (100ug/ml) inhibited the MsC proliferation induced by MsC-derived IL-1; (4) indomethacin (2ug/ml) which inhibited the production of endogenous PGE2, enhanced the MsC proliferation induced by MsC-derived IL-1. The results suggest that there is a self-regulation effect on MsC proliferation by MsC-derived IL-1 and PGE2. Clinically, the beneficial effect of PGE2 should be protected, so that the abuse of indomethacin in the treatment of glomerulonephritis should be avoided.

The heparan sulfate proteoglycan (HSPG) is the major part of sulfated macromolecules synthesized by the cultured rat GECs, and plays an important role in maintaining the glomerular charge-selective function. We have investigated the effects of lipopolysaccharide (LPS, 6.25ng/ml), human recombinant interleukin-2, (HrIl-2, 2.5u/ml), and protamine sulfate (PtS, 100μg/ml) on the proliferation of rat GEC and incorporation of 35 into cell layers in vitro. A method of 3 H-TdR and 35 S-Na₂SO₄ dual isotope labelling technique was used. Statistical analysis was done using analysis of variance for both 3 H-TdR uptake and 35 incorporation, and analysis of variance only for the latter.

These results show that LPS, HrIL-2 and PtS inhibited the proliferation of rat GECs. HrIL-2 also directly inhibited the incorporation of 35 into cell layers, but the roles of LPS and PtS, which decreased 35 -content, only came from their inhibition effects on cell proliferation. We suppose that the decreased production of HSPG by GECs, may contribute to the development of proteinuria.