| First Author | Sen E | Year | 1998 |
| Journal | Scand J Immunol | Volume | 47 |
| Issue | 5 | Pages | 431-5 |
| PubMed ID | 9627126 | Mgi Jnum | J:48242 |
| Mgi Id | MGI:1267008 | Doi | 10.1046/j.1365-3083.1998.00320.x |
| Citation | Sen E, et al. (1998) Immunobiological studies on experimental visceral Leishmaniasis. V. The I-A(Bm12) mutation specifies resistance to infection. Scand J Immunol 47(5):431-5 |
| abstractText | The I-A(Bm12) mutation of the I-A beta subunit converted Leishmania donovani-susceptible C57BL/6 (B6) mice into the relatively resistant B6C-H-2 Bm12 (Bm12) strain. The relative resistance was reflected not only in the reduced splenic and hepatic parasite burden in Bm12 (compared with B6) but also by the ability of Bm12 mice to mount a T-cell proliferative response to parasite antigens. Assay of antileishmanial antibody (immunoglobulin G (IgG)(2a) and IgG(1)) in the sera of infected mice showed that in Bm12 mice the predominant isotype was IgG(2a), rather than IgG(1), whereas a similar level of both isotypes were found in B6 mice. From the serum immunoglobulin isotype titre it appeared that the antileishmanial T-cell response was biased towards a T helper (Th) 1 response in Bm12 mice whereas it was a mixed Th1 and Th2 response in B6 mice. These observations provide credence to the notion that polymorphism in class II major histocompatibility complex (MHC) molecules is responsible for the difference in the disease phenotype. |
