A defining feature of vertebrate immunity is the acquisition of immunological memory, which confers enhanced protection against pathogens by mechanisms that are incompletely understood. Here, we compared responses by virus-specific naive T cells (T-N) and central memory T cells (T-CM) to viral antigen challenge in lymph nodes (LNs). In steady-state LNs, both T cell subsets localized in the deep T cell area and interacted similarly with antigen-presenting dendritic cells. However, upon entry of lymph-borne virus, only T-CM relocalized rapidly and efficiently toward the outermost LN regions in the medullary, interfollicular, and subcapsular areas where viral infection was initially confined. This rapid peripheralization was coordinated by a cascade of cytokines and chemokines, particularly ligands for T-CM-expressed CXCR3. Consequently, in vivo recall responses to viral infection by CXCR3-deficient T-CM were markedly compromised, indicating that early antigen detection afforded by intranodal chemokine guidance of T-CM is essential for efficient antiviral memory.

Chemokine Guidance of Central Memory T Cells Is Critical for Antiviral Recall Responses in Lymph Nodes / Sung, Jh; Zhang, H; Moseman, Ea; Alvarez, D; Iannacone, M; Henrickson, Se; de la Torre, Jc; Groom, Jr; Luster, Ad; von Andrian, Uh. - In: CELL. - ISSN 0092-8674. - 150:6(2012), pp. 1249-1263. [10.1016/j.cell.2012.08.015]

Chemokine Guidance of Central Memory T Cells Is Critical for Antiviral Recall Responses in Lymph Nodes

Iannacone M;
2012-01-01

Abstract

A defining feature of vertebrate immunity is the acquisition of immunological memory, which confers enhanced protection against pathogens by mechanisms that are incompletely understood. Here, we compared responses by virus-specific naive T cells (T-N) and central memory T cells (T-CM) to viral antigen challenge in lymph nodes (LNs). In steady-state LNs, both T cell subsets localized in the deep T cell area and interacted similarly with antigen-presenting dendritic cells. However, upon entry of lymph-borne virus, only T-CM relocalized rapidly and efficiently toward the outermost LN regions in the medullary, interfollicular, and subcapsular areas where viral infection was initially confined. This rapid peripheralization was coordinated by a cascade of cytokines and chemokines, particularly ligands for T-CM-expressed CXCR3. Consequently, in vivo recall responses to viral infection by CXCR3-deficient T-CM were markedly compromised, indicating that early antigen detection afforded by intranodal chemokine guidance of T-CM is essential for efficient antiviral memory.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11768/104000
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