Antigen‐induced inhibition of autoimmune response to rat male accessory glands: distinct characteristics of I‐A‐ and I‐E‐positive peritoneal cells

Abstract

The present report describes different aspects of two populations of peritoneal cells (PC) obtained from rats injected i.p. 2 h or 24 h previously with a suppressor dose of a purified fraction (FI) of rat male accessory glands (RAG) (FI-PC2h and FI-PC24h, respectively). The FI-PC2h, which are mainly I-E (OX17) positive and can suppress the autoimmune response to RAG autoantigens, have an elevated phagocytic activity against Candida albicans and capacity to reduce the dye nitroblue tetrazolium. In contrast, FI-PC24h, which are mainly I-A (OX6) positive and can potentiate the autoimmunity to RAG autoantigens, have a diminished capacity to reduce the dye and a diminished phagocytic activity. Moreover, the Toxoplasma gondii appear to have a different effect on both populations. The parasites can invade FI-PC2h while FI-PC24h offer resistance to T. gondii aggression. FI-PC2h cultured during 22 h (FI-PC2-24h in vitro), or PC obtained from syngeneic recipients injected i.p. 22 h previously with FI-PC2h (FI-PC2-24h in vivo) show, as FI-PC2h, an increase of the I-E+ cells and capacity to induce suppression of the delayed-type hypersensitivity response to RAG autoantigens when they are injected to syngeneic rats 10 and 3 days prior to the immunization with chemically modified (diazotized arsanilic and sulfanilic acid) RAG in complete Freund's adjuvant. The PC obtained 24 h after injection of irradiated rats with N-PC plus FI show an increase of I-E+ cells whereas an enhancement of I-A+ cells can be observed when the PC are obtained 24 h after injection of irradiated and bone marrow-reconstituted rats with N-PC plus FI. These findings appear to indicate that FI-PC2h and FI-PC24h are functionally different and that the population obtained 24 h after injection of FI of RAG could not originate from either the population present 2 h after injection of FI of RAG injection nor from normal PC. They appear to require bone marrow precursors.

Experimental autoimmune encephalomyelitis: Antigen-induced inhibition of biochemical and immunohistological alterations

“…In this regard, we have previously achieved prevention of EAE in Wistar rats by i.p. administration of soluble MBP or whole BM prior to induction of the disease by sensitization with BM in CFA (Rivero et al, 1995(Rivero et al, , 1996. This study extends the preceding work and demonstrates that administration of myelin antigens in a nonimmunogenic form can also suppress CNS biochemical and histological alterations.…”

“…EAE is a complex phenomenon in which the clinical manifestations appear to be the consequence of various immunological factors directed to some specific myelin as well as neuronal constituents. The results obtained using the described antigen-specific inhibition of EAE indicate that suppression of the clinical manifestations and cellular immunity to MBP (Rivero et al, 1995(Rivero et al, , 1996 can be associated with the absence of the CNS histological and biochemical alterations characteristic of the disease.…”

“…Coincidentally, previous results showed that in addition to reduction in clinical severity, i.p. treatment with myelin antigens prior to immunization determined a significant decrease in the in vitro proliferative responses of spleen lymphocytes to MBP (Rivero et al, 1995(Rivero et al, , 1996.…”

“…Using another experimental model of autoimmunity against rat male sex accessory glands induced by immunization with a chemically modified accessory gland saline extract (MRAG) in complete Freund's adjuvant (CFA), we have previously shown that a purified fraction of rat male accessory glands intraperitoneally administered in low doses and soluble form prevents the cellular and humoral autoimmune response when animals are subsequently challenged with MRAG in CFA (Ferro et al , 1985(Ferro et al , , 1990Rivero et al, 199 1). Application of a similar experimental model to EAE demonstrated inhibition of the clinical signs of the disease with a concurrent suppression of the proliferative response of mononuclear cells to MBP (Rivero et al, 1995(Rivero et al, , 1996.…”

Regulatory role of OX22high T cells in mercury-induced autoimmunity in the brown Norway rat.

“…Responsiveness in the mouse to HgC12 is linked to the MHC class II A ~ molecule, and coexpression of the other class II molecule (the E molecule) in an A ~ strain decreases responsiveness (34). There are also examples in the rat in which responses channelled via the two class II molecules appear to have opposing immunoregulatory effects (38,39). Whether this applies to the response to HgC12 in the rat is unknown, but clearly there is ample precedent for the differential activation of regulatory subsets by different MHC molecules, both between and within particular haplotypes.…”