Lymphokine-activated killer cells, natural killer cells and cytokines

Perussia, Bice

doi:10.1016/0952-7915(91)90076-d

Cited by 159 publications

(77 citation statements)

References 42 publications

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“…NK cells produce IFN-7 [7], as well as other eytokines such as tumour necrosis factor-alpha (TNF-rv). granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-3 (for review see [9] and Toxopta.wui gondii [22]. Although NK cells have been identified in lesion biop-sies from /Lt'/.v/jmoHifl-infected humans [23].…”

Section: Discussionmentioning

confidence: 99%

Response ofscidmice to establishment ofLeishmania majorinfection

Guy

Belosevic

1995

Clinical and Experimental Immunology

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SUMMARYThe initiation o^ Leishmania major \n^e:c\\ox\ in su.sceptible BALB/c mice is regulated by inlerferongamma (lKN-->). To examine further the mechanisms of lFN-7-dependent regulation of the establishment of L. major, we studied the characteristics of the infection in severe combined immunodeticient {scid) mice. In the lirst 2 weeks of infection, we observed a delay in the development of the lesions in the footpads and lower numbers of parasites in scid compared with BALB/c mice. By week 5 after infection, the size ofthe leishmanial lesion was similar in both strains of mice, but the number of parasites in scid mice was 100-fold higher than in BALB/c. Treatment with anti-IFN-7 during the establishment of L. major did not alter the course of infection in .Wi^mice, while it exacerbated lesion development in BALB/c mice. Macrophages from scid mice were unable to kill L. major when stimulated with IFN--) in vitro, and produced lower levels of nitric oxide compared with macrophages from susceptible BALB/c or the resistant C57B1/ 6 mice. We examined whether delayed lesion development in.«((/mice was due to their inability to mouni appropriate inflammatory responses. While significantly fewer nucleated cells were present in the footpads of .vc/J mice compared with BALB/c. 2 and 3 weeks alter infection, no difference in inflammatory response between scid and BALB/c mice was observed in response to L. major antigen in the footpads. In contrast, there was a dramatic increase in the number ofcells in ihe popliteal lymph nodes of BALB/c mice. Decreased inflammatory responses oWscid mice in Ihe footpad (at (he site of infection) may contribute to slower development of leishmanial lesions during the first 2 weeks of infection.

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Section: Discussionmentioning

confidence: 99%

Response ofscidmice to establishment ofLeishmania majorinfection

Guy

Belosevic

1995

Clinical and Experimental Immunology

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“…NK cells have potent cytotoxic functions and are efficient producers of several cytokines including IFN-g, TNF-a, and GM-CSF [2]. The latter contribute to the immunoregulatory properties of NK cells, which affect anti-microbial and anti-tumor responses as well as the outcome of many autoimmune and hypersensitivity reactions [3].…”

Section: Introductionmentioning

confidence: 99%

Plasmacytoid dendritic cell‐induced migration and activation of NK cells in vivo

Persson

Chambers

2010

Eur J Immunol

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NK cells are cytotoxic cells of the innate immune system. They have been found to be critical in the defense against infections and also against some tumors. Recent studies have shown that NK cells require signals from accessory cells to induce their recruitment and activation at the site of infection or tumor growth. In this study, we examined whether plasmacytoid DC (pDC) could recruit and activate NK cells in vivo. When CpG-stimulated pDC were injected i.p. to C57BL/6 mice, they efficiently recruited NK cells, a process that was dependent on NK cell CXCR3 and CD62L and in part on CCR5. NK cells isolated from the peritoneum of mice inoculated with TLR7/8 or TLR9-stimulated pDC exhibited greater cytotoxicity against YAC-1 tumor cells than NK cells recovered from mice inoculated with control pDC. The present results are discussed in relation to pDC-induced NK cell migration and activation in vivo.Key words: Cellular activation . Cell migration . Costimulatory moleculers . Dendritic cells . NK cell IntroductionNK cells are lymphocytes of the innate immune system that play a crucial role in the early host defense against infections and some tumors [1]. NK cells have potent cytotoxic functions and are efficient producers of several cytokines including IFN-g, TNF-a, and GM-CSF [2]. The latter contribute to the immunoregulatory properties of NK cells, which affect anti-microbial and anti-tumor responses as well as the outcome of many autoimmune and hypersensitivity reactions [3]. By their cytotoxicity and cytokine production, NK cells can affect CTL responses in infection and tumor models as well as B-cell responses [4][5][6][7][8]. NK cells are found in both nonlymphoid and lymphoid tissues including lung, liver, blood, spleen, and LN [9]. Several studies have demonstrated that NK cells migrate to different tissues in response to stimuli, such as allergic responses, infections, or tumor growth [10][11][12][13][14][15][16][17][18][19]. Four chemokine receptors, CCR2, CCR5, CXCR3 and CX3CR1, have been shown to be particularly important for mouse NK-cell migration to various inflammatory stimulus [4,9]. However, other molecules such as CD62L, IFN-g, sphingosine 1-phosphate receptor, and TNF-a are also important for the NKcell migration in mice. For example, blocking CD62L with Ab prevents the egress of NK cells from blood into LN [4]. IFN-g modulates migration by inducing the production of CXCL10 (IP10) [20]. Thus, mice deficient in IFN-g also exhibit reduced CXCL10 production. In mice lacking sphingosine 1-phosphate receptor, NK cells accumulate in the LN and bone marrow while being absent from blood, spleen, or lungs [21]. Thus chemokine activation of NK cells is important for their recruitment to inflammatory sites. In both mice and humans, two main types of ''DC'' exist, conventional DC (cDC), including both lymphoid tissue-resident DC and migratory DC, and so-called plasmacytoid DC (pDC). In mice, cDC in the spleen can be further subdivided into the CD8a 1 and CD8a À populations. The former are involved in crosspr...

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“…We showed that male Ag-specific T cells developed in athymic male mice were also IL-2R␤ ϩ (7). Other than extrathymically developed T cells, NK cells express low affinity IL-2R and are known to respond to exogenous IL-2 (16). IL-15 is a novel cytokine that utilizes IL-2 receptors to exert biological activities (17).…”

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confidence: 99%

TCR-Independent Activation of Extrathymically Developed, Self Antigen-Specific T Cells by IL-2/IL-15

Yamada

Nakamura

Matsuzaki

et al. 2000

The Journal of Immunology

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Naive intrathymically developed T cells, which express foreign Ag-specific TCR, do not express IL-2R. After antigenic stimulation, they express high affinity IL-2R, which enables IL-2 to be used as an autocrine growth factor. On the contrary, extrathymically developed T cells, which express self Ag-specific TCR but are unresponsive to antigenic stimulation, spontaneously express low affinity IL-2R. In this study, we compared the responses of these two subsets of T cells to IL-2R stimulation and examined the influences of TCR-mediated signaling on the responses. IL-2 or IL-15 augmented the proliferative response of Ag-stimulated, intrathymically developed T cells. On the other hand, extrathymically developed T cells proliferated in response to IL-2 or IL-15, independently of Ag stimulation. Furthermore, both IL-2 and IL-15 induced IFN-γ production of these T cells, which is strikingly augmented by the presence of IL-12. These results revealed functional differences between intrathymically developed, foreign Ag-specific T cells and extrathymically developed, self Ag-specific T cells. The latter can be activated by some inflammatory cytokines, in an Ag-independent manner, similar to NK cells.

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Lymphokine-activated killer cells, natural killer cells and cytokines

Cited by 159 publications

References 42 publications

Response ofscidmice to establishment ofLeishmania majorinfection

Response ofscidmice to establishment ofLeishmania majorinfection

Plasmacytoid dendritic cell‐induced migration and activation of NK cells in vivo

TCR-Independent Activation of Extrathymically Developed, Self Antigen-Specific T Cells by IL-2/IL-15

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