Lung-resident CD4⁺ T cells are sufficient for IL-4Rα-dependent recall immunity to Nippostrongylus brasiliensis infection
Research output: Contribution to journal › Article
Colleges, School and Institutes
- International Centre for Genetic Engineering and Biotechnology/Institute of Infectious Diseases and Molecular Medicine, Health Science Faculty, University of Cape Town, Cape Town, South Africa.
- Department of Human Biology, Health Science Faculty, University of Cape Town, Cape Town, South Africa.
Immunity to Nippostrongylus brasiliensis reinfection requires pulmonary CD4⁺ T-cell responses. We examined whether secondary lymphoid recruited or pre-existing lung CD4⁺ T-cell populations coordinated this immunity. To do this, we blocked T-cell egress from lymph nodes using Fingolimod (FTY720). This impaired host ability to resolve a primary infection but did not change effectiveness of recall immunity. Associated with this effective recall immunity was the expansion and T helper type 2 polarization of a pre-existing pulmonary CD4⁺ T-cell population. LTβR-Ig (lymphotoxin beta-receptor fusion protein)-mediated disruption of stromal cell organization of immune cells did not disrupt this recall immunity, suggesting that protection was mediated by a pulmonary interstitial residing CD4⁺ T-cell population. Adoptive transfer of N. brasiliensis-experienced pulmonary CD4⁺ T cells from FTY720-treated wild-type or T-cell interleukin (IL)-4Rα-deficient mice demonstrated protection to be IL-4Rα dependent. These results show that pre-existing CD4⁺ T cells can drive effective recall immunity to N. brasiliensis infection independently of T-cell recruitment from secondary lymphoid organs.
|Number of pages||10|
|Early online date||19 Jun 2013|
|Publication status||Published - Mar 2014|
- Animals, CD4-Positive T-Lymphocytes, Cell Movement, Disease Models, Animal, Gene Expression, Immunologic Memory, Interleukin-4 Receptor alpha Subunit, Lung, Lymph Nodes, Mice, Mice, Knockout, Nippostrongylus, Strongylida Infections, Journal Article, Research Support, Non-U.S. Gov't, CD4-positive T cells, Immunological memory, Parasite host response, Parasitic infection