| First Author | Karulin AY | Year | 2002 |
| Journal | J Immunol | Volume | 168 |
| Issue | 2 | Pages | 545-53 |
| PubMed ID | 11777945 | Mgi Jnum | J:313292 |
| Mgi Id | MGI:6705200 | Doi | 10.4049/jimmunol.168.2.545 |
| Citation | Karulin AY, et al. (2002) Indirect IL-4 pathway in type 1 immunity. J Immunol 168(2):545-53 |
| abstractText | Recall Ag-specific IL-4 was detected in the spleen and in the blood, but not in lymph nodes of mice in which polarized type 1 immunity was induced. This IL-4 was not produced by T cells, but soluble factors secreted by the recall Ag-activated T cells, including IL-3, triggered cells of the innate immune system, primarily mast cells, to secrete IL-4. This notion has profound implications for immunodiagnostics: the detection of apparently recall Ag-specific IL-4 does not necessarily reflect the presence of Th2 or Th0 memory T cells with long-term cytokine commitment as is of interest for assessing adoptive immunity. We found that in vivo the indirect IL-4 pathway did not suffice to trigger IgE isotype switching, but promoted IgG1 production and inhibited type 1 T cell differentiation. Therefore, the indirect IL-4 pathway can explain partial type 2 immune response phenotypes in vivo in face of unipolar Th1 T cell immunity. The representation of mast cells in different tissues may explain why immune responses in certain organs are more type 2 biased. Therefore, the indirect pathway of IL-4 production represents a novel type of interaction between the innate and the adoptive immune system that can contribute to the outcome of host defense and immune pathology. |
