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Updated: Jan 25, 2026
Measuring Bacterial Load and Immune Responses in Mice Infected with Listeria monocytogenes
Published on: August 9, 2011
CD160 Stimulates CD8+ T Cell Responses and Is Required for Optimal Protective Immunity to Listeria monocytogenes
Catherine L Tan1,2, Michael J Peluso1,2, Jefte M Drijvers1,2
1Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115.
Insights
CD160 costimulatory signals enhance CD8+ T cell functions crucial for clearing oral Listeria monocytogenes infections. Mice lacking CD160 show impaired bacterial clearance due to compromised T cell responses.
Area of Science:
- Immunology
- Microbial Pathogenesis
- Cellular Immunology
Background:
- The precise role of CD160 on CD8+ T cells in immune responses is debated, with conflicting evidence suggesting both coinhibitory and costimulatory functions.
- Previous studies indicated CD160's role in Natural Killer (NK) cell activity, but its impact on T cell-mediated immunity, particularly during bacterial infections, remained largely unexplored.
Purpose of the Study:
- To elucidate the function of CD160 on CD8+ T cells in the context of mucosal bacterial infection.
- To determine whether CD160 plays a costimulatory or coinhibitory role in CD8+ T cell effector functions during oral Listeria monocytogenes infection.
Main Methods:
- Comparative analysis of oral Listeria monocytogenes clearance in wild-type (WT) and CD160 knockout (CD160-/-) mice.
- Assessment of immune cell populations, including intraepithelial lymphocytes and splenic CD8+ T cells, for effector function markers like granzyme B, IFN-γ, and TNF-α.
- Adoptive transfer experiments using CD8+ T cells from WT and CD160-/- mice into RAG-/- recipients to evaluate their protective capacity.
Main Results:
- CD160-/- mice exhibited significantly impaired clearance of oral L. monocytogenes compared to WT littermates.
- The absence of CD160 led to compromised CD8+ T cell effector functions, evidenced by reduced granzyme B, IFN-γ, and TNF-α production.
- Adoptive transfer of CD160-/- CD8+ T cells resulted in higher mortality and bacterial burden in recipient mice, confirming a critical costimulatory role for CD160.
Conclusions:
- CD160 functions as a costimulatory molecule for CD8+ T cells, enhancing their effector functions necessary for controlling oral bacterial infections.
- The findings highlight CD160's importance in orchestrating protective immunity against mucosal bacterial pathogens through modulation of CD8+ T cell responses.
Abstract:
CD160 promotes NK cell cytotoxicity and IFN-γ production, but the function of CD160 on CD8+ T cells remains unclear with some studies supporting a coinhibitory role and others a costimulatory role. In this study, we demonstrate that CD160 has a costimulatory role in promoting CD8+ T cell effector functions needed for optimal clearance of oral Listeria monocytogenes infection. CD160-/- mice did not clear oral L. monocytogenes as efficiently as wild type (WT) littermates. WT RAG-/- and CD160-/- RAG-/- mice similarly cleared L. monocytogenes, indicating that CD160 on NK cells does not contribute to impaired L. monocytogenes clearance. Defective L. monocytogenes clearance is due to compromised intraepithelial lymphocytes and CD8+ T cell functions. There was a reduction in the frequencies of granzyme B-expressing intraepithelial lymphocytes in L. monocytogenes-infected CD160-/- mice as compared with WT littermate controls. Similarly, the frequencies of granzyme B-expressing splenic CD8+ T cells and IFN-γ and TNF-α double-producer CD8+ T cells were significantly reduced in L. monocytogenes-infected CD160-/- mice compared with WT littermates. Adoptive transfer studies showed that RAG-/- recipients receiving CD160-/- CD8+ T cells had a higher mortality, exhibited more weight loss, and had a higher bacterial burden compared with RAG-/- recipients receiving WT CD8+ T cells. These findings demonstrate that CD160 provides costimulatory signals to CD8+ T cells needed for optimal CD8+ T cell responses and protective immunity during an acute mucosal bacterial infection.
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