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Essential role of lymph nodes in contact hypersensitivity revealed in lymphotoxin-alpha-deficient mice.

Authors: Rennert, PD  Hochman, PS  Flavell, RA  Chaplin, DD  Jayaraman, S  Browning, JL  Fu, YX 
Citation: Rennert PD, etal., J Exp Med. 2001 Jun 4;193(11):1227-38.
Pubmed: (View Article at PubMed) PMID:11390430

Lymph nodes (LNs) are important sentinal organs, populated by circulating lymphocytes and antigen-bearing cells exiting the tissue beds. Although cellular and humoral immune responses are induced in LNs by antigenic challenge, it is not known if LNs are essential for acquired immunity. We examined immune responses in mice that lack LNs due to genetic deletion of lymphotoxin ligands or in utero blockade of membrane lymphotoxin. We report that LNs are absolutely required for generating contact hypersensitivity, a T cell-dependent cellular immune response induced by epicutaneous hapten. We show that the homing of epidermal Langerhans cells in response to hapten application is specifically directed to LNs, providing a cellular basis for this unique LN function. In contrast, the spleen cannot mediate contact hypersensitivity because antigen-bearing epidermal Langerhans cells do not access splenic white pulp. Finally, we formally demonstrate that LNs provide a unique environment essential for generating this acquired immune response by reversing the LN defect in lymphotoxin-alpha(-/)- mice, thereby restoring the capacity for contact hypersensitivity.


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RGD Object Information
RGD ID: 8548819
Created: 2014-03-20
Species: All species
Last Modified: 2014-03-20
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.