| First Author | Carter T | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 8 | Pages | 5116-23 |
| PubMed ID | 17404294 | Mgi Jnum | J:145279 |
| Mgi Id | MGI:3834066 | Doi | 10.4049/jimmunol.178.8.5116 |
| Citation | Carter T, et al. (2007) Mannose-binding lectin A-deficient mice have abrogated antigen-specific IgM responses and increased susceptibility to a nematode infection. J Immunol 178(8):5116-23 |
| abstractText | To investigate the role of mannose-binding lectin-A (MBL-A) in protection against infectious disease, MBL-A(-/-)-deficient mice were generated. Using a well-characterized mouse model of human filarial nematode infection, nematode survival and protective immune responses were tested in vivo. Blood-borne Brugia malayi microfilariae survived for significantly longer time periods in MBL-A(-/-) than in wild-type (WT) mice. However, no differences in either splenic cytokine responses or induction of leukocytes in the blood were observed. A profound abrogation of Ag-specific IgM levels was measured in B. malayi-infected MBL-A(-/-) mice, and some IgG isotypes were higher than those observed in WT animals. To establish whether there was a defect in Ab responses per se in MBL-A(-/-) mice or the effect was specific to filarial infection, we immunized these mice with OVA or a carbohydrate-free protein. Significantly, Ag-specific IgM responses were defective to both of these Ags, and Ag-specific IgG responses were largely unaffected. Furthermore, in naive mice, total IgM levels did not differ between MBL-A(-/-) and WT mice. This article describes the first demonstration that MBL-A may function independently of MBL-C and suggests that MBL-A, like other C-type lectins and members of the complement cascade, is intimately involved in the priming of the humoral Ab response. |
