CD30 Is Required for CCL21 Expression and CD4 T Cell Recruitment in the Absence of Lymphotoxin Signals
- Authors
- Bekiaris, Vasileios; Gaspal, Fabrina; Kim, Mi-Yeon; Withers, David R.; McConnell, Fiona M.; Anderson, Graham; Lane, Peter J. L.
- Issue Date
- 15-Apr-2009
- Publisher
- AMER ASSOC IMMUNOLOGISTS
- Citation
- JOURNAL OF IMMUNOLOGY, v.182, no.8, pp.4771 - 4775
- Journal Title
- JOURNAL OF IMMUNOLOGY
- Volume
- 182
- Number
- 8
- Start Page
- 4771
- End Page
- 4775
- URI
- http://scholarworks.bwise.kr/ssu/handle/2018.sw.ssu/15849
- DOI
- 10.4049/jimmunol.0803481
- ISSN
- 0022-1767
- Abstract
- Lymphoid tissue inducer cells express a diverse array of tumor necrosis family ligands, including those that bind CD30 and the lymphotoxin 13 receptor. Both of these signaling pathways have been linked with B/T segregation in the spleen. In this study, we have dissected a lymphotoxin-independent CD30-dependent signal for the induction of expression of the T zone chemokine, CCL21. Reduced expression of CCL21 due to CD30 deficiency was functionally significant: mice deficient in both lymphotoxin and CD30 (dKO) signals had significantly smaller accumulations of lymphocytes in their splenic white pulp areas, with no evidence of focal aggregation of T cells. Furthermore, recruitment of wild-type CD4 T cells was poor in dKO mice compared with both wild-type or lymphotoxin-deficient mice. Phylogeny suggests that CD30 signals predated those through the lymphotoxin 0 receptor. We suggest that CD30 signals from lymphoid tissue inducer cells were a primitive mechanism to recruit and prime CD4 T cells. This would have been a stepping stone in the evolution of the highly organized lymphotoxin dependent B and T white pulp areas within which CD4-dependent memory Ab responses now develop. The Journal of Immunology, 2009, 182: 4771-4775.
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