Profiles of Th1 and Th2 cytokines after primary and secondary infection bySchistosoma mansoni in the semipermissive rat host

Citation
C. Cetre et al., Profiles of Th1 and Th2 cytokines after primary and secondary infection bySchistosoma mansoni in the semipermissive rat host, INFEC IMMUN, 67(6), 1999, pp. 2713-2719
Citations number
44
Categorie Soggetti
Immunology
Journal title
INFECTION AND IMMUNITY
ISSN journal
00199567 → ACNP
Volume
67
Issue
6
Year of publication
1999
Pages
2713 - 2719
Database
ISI
SICI code
0019-9567(199906)67:6<2713:POTATC>2.0.ZU;2-V
Abstract
In contrast to most mouse strains, rats eliminate the primary schistosome b urden around 4 weeks postinfection and subsequently develop protective immu nity to reinfection. In rat schistosomiasis, we have shown predominant expr ession of a Th2-type cytokine response at the mRNA level after primary infe ction. In the present study, we showed a significant increase in interleuki n-4 (IL-4) mRNA expression in inguinal lymph nodes early after a secondary infection. IL-5 mRNA expression showed a significant increase at days 2 and 4 postreinfection in the spleen and lymph nodes, respectively. We did not detect any gamma interferon (IFN-gamma) mRNA after a challenge infection. A nalysis of cytokine secretion by stimulated spleen cells after a primary in fection showed predominant expression of IL-4 with maximum production on da y 21, accompanied by production of IL-5 from day 11 to day 67. A significan t increase in IFN-gamma secretion was detected at day 21. Analysis of immun oglobulin G2b (IgG2b) and IgG2c (Th1-related isotypes) showed undetectable levels of IgG2b, but detectable levels of specific IgG2c antibodies were ob served from day 42. The analysis of Th2-related isotypes showed high specif ic IgG1 and IgG2a antibody titers from day 29. After a secondary infection, only IL-4 and IL-5 secretion was sustained. This is supported by the incre ased production of Th2-related isotypes. These findings showed that S. mans oni infection can drive Th2 responses in rats in the absence of egg product ion which is required to induce a Th2 response in mice and are in favor of the role of Th2-type cytokines in protective immunity against reinfection.