| First Author | Rempel JD | Year | 2000 |
| Journal | Eur J Immunol | Volume | 30 |
| Issue | 2 | Pages | 347-55 |
| PubMed ID | 10671189 | Mgi Jnum | J:115321 |
| Mgi Id | MGI:3691385 | Doi | 10.1002/1521-4141(200002)30:2<347::AID-IMMU347>3.0.CO;2-H |
| Citation | Rempel JD, et al. (2000) Endogenous IL-12 synthesis is not required to prevent hyperexpression of type 2 cytokine and antibody responses. Eur J Immunol 30(2):347-55 |
| abstractText | Endogenous IL-12 production is hypothesized to play an essential role preventing spontaneous expression of type 2 responses, acting as a natural inhibitor limiting development of immediate hypersensitivity. Here, IL-12-deficient p35(- / -) and p40(- / -) mice were used to examine the role of endogenous IL-12 and p40 homodimer during in vivo development of exogenous antigen-driven responses. In the absence of deliberate immunization, IL-12-deficient mice exhibited greatly reduced serum IgG2a but IgG1 / IgE levels no higher than controls. Immunization to elicit polarized ovalbumin-specific type 1 or type 2 dominant responses, or using Trichinella spiralis extract in the absence of adjuvants, led to IFN-gamma production of approximately 10 % of C57BL / 6 controls yet the kinetics and intensity of primary and secondary type 2 cytokine (IL-4, IL-5, IL-13) and antibody (IgG1, IgE) responses, as well as functional IL-12 receptor expression, were consistently unaltered. Thus, while IL-12 provides an important positive signal for Th1 development, antigen exposure in its absence does not lead to generalized enhancement of type 2 cytokine or antibody responses. The data argue that endogenous IL-12 production is not required as a constitutive negative regulator limiting induction or expression of type 2 effector responses. |
