505 Activation of NK T cells promote the inflammatory tumor microenvironment and control the growth of solid tumor

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A540-A540
Author(s):  
Sourav Paul ◽  
Amrita Mishra ◽  
Sushanta Chhatar ◽  
Girdhari Lal ◽  
Girdhari Lal
Keyword(s):  
T Cells ◽  
Tumor Microenvironment ◽  
Inflammatory Cytokines ◽  
Nkt Cells ◽  
Th1 Cells ◽  
Inkt Cells ◽  
M1 Macrophages ◽  
Ifn Gamma ◽  
Nk T Cells ◽  
Secondary Lymphoid Organs

BackgroundType I NK T cells, also known as iNKT cells, can recognize self or microbial lipids presented through CD1d molecules on antigen-presenting cells. Activation of NKT cells induces inflammatory cytokines and help in mounting anti-tumor immunity. How does stimulation of iNKT cells in vivo alter the tumor microenvironment is not clearly understood.MethodsC57BL/6 mice were given a subcutaneous injection of B16F10 melanoma cell line (1 X 106 cells). Mice were given intraperitoneal injection of alpha-galactosylceramide (a-GalCer, a ligand for iNKT cells; 2 microgram/injection) on day +1, +5, +10, +15 and +20. NK cells, Gr1+ cells and F4/80+ macrophages in mice were depleted using cell-specific antibodies. The growth of tumors was monitored, and immune cells were characterized using flow cytometry and immunofluorescence staining. Student’s t-test and one-way ANOVA were used for statistical analysis.ResultsOur results showed that intratumoral NK T cells had significantly low expression of CD25, CD69, CD122, and IFN-gamma receptor molecules and produced lower inflammatory cytokines (IFN-gamma, TNF-alpha, and GM-CSF) as compared to splenic NK T cells. The soluble factor produced by B16F10 cells reduces the expression of these cytokines and cytokine receptors in vitro on the NK T cells purified from the spleen. Treatment of tumor-bearing mice with a-GalCer significantly increased the IFN-gamma-producing NK T cells, CD8+ T cells, and effector Th1 cells in secondary lymphoid organs, and tumors, also significantly reduced the tumor growth. Furthermore, a-GalCer treatment significantly increased the iNOS+CD206- M1-macrophages and reduced the iNOS-CD206+ M2-macrophages in the spleen and tumor. The depletion of F4/80+ macrophages prevented the a-GalCer-induced reduction of tumor growth.ConclusionsOur results showed that tumor produced soluble factors alter the phenotype of NK T cells. Activation of NKT cells with a-GalCer promotes the M1-macrophages, and effector CD8+ T cells, Th1 cells in the secondary lymphoid organs and tumor microenvironment. This finding suggests that activation of NKT cells may provide an effective anti-tumor response.AcknowledgementsThis work was supported by the Science and Engineering Research Board grant (EMR/2016/007108) and SwarnJayanti Fellowship (DST/SJF/LSA-01/2017–18) from the Department Science and Technology (DST), Government of India.Ethics ApprovalAll the procedures performed in the experiments involving mice were in accordance with the ethical standards of (NCCS) Institutional Ethics Committee of Animals Usage (Approval ID: EAF/B-166/2011 and EAF/B-256/2016).

scholarly journals Type I Natural Killer T Cells as Key Regulators of the Immune Response to Infectious Diseases

2020 ◽  
Vol 34 (2) ◽  
pp. e00232-20
Author(s):  
Nicolás M. S. Gálvez ◽  
Karen Bohmwald ◽  
Gaspar A. Pacheco ◽  
Catalina A. Andrade ◽  
Leandro J. Carreño ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Infectious Diseases ◽  
Natural Killer ◽  
Nkt Cells ◽  
Interleukin 4 ◽  
Type I ◽  
Inkt Cells ◽  
Class I Mhc ◽  
Natural Killer T

SUMMARYThe immune system must work in an orchestrated way to achieve an optimal response upon detection of antigens. The cells comprising the immune response are traditionally divided into two major subsets, innate and adaptive, with particular characteristics for each type. Type I natural killer T (iNKT) cells are defined as innate-like T cells sharing features with both traditional adaptive and innate cells, such as the expression of an invariant T cell receptor (TCR) and several NK receptors. The invariant TCR in iNKT cells interacts with CD1d, a major histocompatibility complex class I (MHC-I)-like molecule. CD1d can bind and present antigens of lipid nature and induce the activation of iNKT cells, leading to the secretion of various cytokines, such as gamma interferon (IFN-γ) and interleukin 4 (IL-4). These cytokines will aid in the activation of other immune cells following stimulation of iNKT cells. Several molecules with the capacity to bind to CD1d have been discovered, including α-galactosylceramide. Likewise, several molecules have been synthesized that are capable of polarizing iNKT cells into different profiles, either pro- or anti-inflammatory. This versatility allows NKT cells to either aid or impair the clearance of pathogens or to even control or increase the symptoms associated with pathogenic infections. Such diverse contributions of NKT cells to infectious diseases are supported by several publications showing either a beneficial or detrimental role of these cells during diseases. In this article, we discuss current data relative to iNKT cells and their features, with an emphasis on their driving role in diseases produced by pathogenic agents in an organ-oriented fashion.

scholarly journals Regulatory interactions between CD45RBhigh and CD45RBlow CD4+ T cells are important for the balance between protective and pathogenic cell-mediated immunity.

1994 ◽  
Vol 179 (2) ◽  
pp. 589-600 ◽  
Author(s):  
F Powrie ◽  
R Correa-Oliveira ◽  
S Mauze ◽  
R L Coffman
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Scid Mice ◽  
Th2 Cells ◽  
Cell Mediated Immunity ◽  
Th1 Cells ◽  
Ifn Gamma ◽  
Th1 Response ◽  
Major Infection

BALB/c mice infected with the intracellular protozoan Leishmania major mount a T helper cell 2 (Th2) response that fails to control growth of the parasite and results in the development of visceral leishmaniasis. Separation of CD4+ T cells into CD45RBhigh and CD45RBlow subsets showed that the L. major-specific Th2 cells were contained within the CD45RBlow population as these cells produced high levels of antigen-specific interleukin 4 (IL-4) in vitro and transferred a nonhealing response to L. major-infected C.B-17 scid mice. In contrast, the CD45RBhighCD4+ population contained L. major-reactive cells that produced interferon gamma (IFN-gamma) in vitro and transferred a healing Th1 response to L. major-infected C.B-17 scid mice. Transfer of the Th1 response by the CD45RBhigh population was inhibited by the CD45RBlow population by a mechanism that was dependent on IL-4. These data indicate that L. major-specific Th1 cells do develop in BALB/c mice, but their functional expression is actively inhibited by production of IL-4 by Th2 cells. In this response, the suppressed Th1 cells can be phenotypically distinguished from the suppressive Th2 cells by the level of expression of CD45RB. Although the CD45RBhigh population mediated a protective response to L. major, C.B-17 scid mice restored with this population developed a severe inflammatory response in the colon that was independent of L. major infection, and was prevented by cotransfer of the CD45RBlow population. The colitis appeared to be due to a dysregulated Th1 response as anti-IFN-gamma, but not anti-IL-4, prevented it. Taken together, the data show that the CD4+ T cell population identified by high level expression of the CD45RB antigen contains cells that mediate both protective and pathogenic Th1 responses and that the reciprocal CD45RBlow population can suppress both of these responses. Whether suppression of cell-mediated immunity is beneficial or not depends on the nature of the stimulus, being deleterious during L. major infection but crucial for control of potentially pathogenic inflammatory responses developing in the gut.

scholarly journals Heterogeneity of helper/inducer T lymphocytes. II. Effects of interleukin 4- and interleukin 2-producing T cell clones on resting B lymphocytes.

1988 ◽  
Vol 167 (4) ◽  
pp. 1350-1363 ◽  
Author(s):  
W H Boom ◽  
D Liano ◽  
A K Abbas
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Th1 Cells ◽  
Specific Class ◽  
Ifn Gamma ◽  
T Cell Clones ◽  
Cell Clones

To compare the helper function of murine T cell clones that secrete IL-2 and IFN-gamma (Th1 cells) or IL-4 and IL-5 (Th2), purified resting B cells were stimulated with F(ab')2 rabbit anti-mouse Ig (RAMG) and rabbit Ig-specific, class II MHC-restricted cloned T cells belonging to the two subsets. Both Th2 clones examined induced strong proliferative responses of B cells in the presence of RAMG, as well as the secretion of IgM and IgG1 antibodies. In contrast, the Th1 clones tested failed to stimulate B cell growth or antibody secretion. Th2-mediated B cell activation was dependent on IL-4 and IL-5, and was also inhibited by IFN-gamma or IFN-gamma produced by Th1 cells present in the same cultures. However, the failure of Th1 cells to help resting B cells could not be reversed with neutralizing anti-IFN-gamma antibody. In addition to this inhibitory effect, IFN-gamma was required for the secretion of IgG2a antibody, particularly when B cells were stimulated with polyclonal activators such as LPS. Finally, both sets of T cell clones secreted lymphokines when stimulated with purified B cells and RAMG. These experiments demonstrate that T cells that differ in lymphokine production also differ in their ability to help B cells as a result of cognate interactions at low concentrations of antigens. Moreover, IL-4, IL-5, and IFN-gamma serve different roles in the T cell-dependent proliferative and differentiative responses of resting B lymphocytes.

scholarly journals Resolution of cutaneous leishmaniasis: interleukin 12 initiates a protective T helper type 1 immune response.

1993 ◽  
Vol 177 (6) ◽  
pp. 1797-1802 ◽  
Author(s):  
J P Sypek ◽  
C L Chung ◽  
S E Mayor ◽  
J M Subramanyam ◽  
S J Goldman ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Enzyme Linked Immunosorbent Assay ◽  
Th1 Cells ◽  
T Helper ◽  
Ifn Gamma ◽  
Lymph Node Cells ◽  
Helper Type

Resistance to Leishmania major in mice is associated with the appearance of distinct T helper type 1 (Th1) and Th2 subsets. T cells from lymph nodes draining cutaneous lesions of resistant mice are primarily interferon gamma (IFN-gamma)-producing Th1 cells. In contrast, T cells from susceptible mice are principally Th2 cells that generate interleukin 4 (IL-4). Although existing evidence is supportive of a role for IFN-gamma in the generation of Th1 cells, additional factors may be required for a protective response to be maintained. A potential candidate is IL-12, a heterodimeric cytokine produced by monocytes and B cells that has multiple effects on T and natural killer cell function, including inducing IFN-gamma production. Using an experimental leishmanial model we have observed that daily intraperitoneal administration at the time of parasite challenge of either 0.33 micrograms IL-12 (a consecutive 5 d/wk for 5 wk) or 1.0 micrograms IL-12 per mouse (only a consecutive 5 d) caused a > 75% reduction in parasite burden at the site of infection, in highly susceptible BALB/c mice. Delay of treatment by 1 wk had less of a protective effect. Concomitant with these protective effects was an increase in IFN-gamma and a decrease in IL-4 production, as measured by enzyme-linked immunosorbent assay of supernatants generated from popliteal lymph node cells stimulated with leishmanial antigen in vitro. The reduction in parasite numbers induced by IL-12 therapy was still apparent at 10 wk postinfection. In addition, we observed that the administration of a rabbit anti-recombinant murine IL-12 polyclonal antibody (200 micrograms i.p. every other day for 25 d) at the time of infection to resistant C57Bl/6 mice exacerbated disease. These effects were accompanied by a shift in IFN-gamma production in vitro by antigen-stimulated lymph node cells indicative of a Th2-like response. These findings suggest that IL-12 has an important role in initiating a Th1 response and protective immunity.

scholarly journals CD4+ effector cells default to the Th2 pathway in interferon gamma-deficient mice infected with Leishmania major.

1994 ◽  
Vol 179 (4) ◽  
pp. 1367-1371 ◽  
Author(s):  
Z E Wang ◽  
S L Reiner ◽  
S Zheng ◽  
D K Dalton ◽  
R M Locksley
Keyword(s):  
T Cells ◽  
Interferon Gamma ◽  
Knockout Mice ◽  
Leishmania Major ◽  
Interleukin 4 ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Wild Type ◽  
Cd4 Cells ◽  
Ifn Gamma

Mice with homologous disruption of the interferon gamma (IFN-gamma) gene on the C57BL/6 background were infected with Leishmania major and the immune response assessed. In contrast to wild-type or heterozygous knockout mice, deficient animals were unable to restrict growth of the parasite and suffered lethal infection over 6-8 wk. Although wild-type and heterozygous littermates developed CD4+ cells that contained transcripts for IFN-gamma and lymphotoxin, typical of T helper type 1 (Th1) cells, the knockout mice developed CD4+ cells that contained transcripts for interleukin 4 (IL-4), IL-5, and IL-13, typical of Th2 cells. ELISPOT assays confirmed the reciprocal patterns of IFN-gamma or IL-4 production by T cells in similar frequencies in the respective groups of mice, and antibody analysis confirmed the presence of Th2-mediated isotype switching in the knockout mice. These data suggest that CD4+ T cells that normally respond to antigens by differentiation to Th1 cells default to the Th2 pathway in the absence of endogenous IFN-gamma.

scholarly journals Deciphering the Prognostic Implications of the Components and Signatures in the Immune Microenvironment of Pancreatic Ductal Adenocarcinoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Rong Tang ◽  
Xiaomeng Liu ◽  
Chen Liang ◽  
Jie Hua ◽  
Jin Xu ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Microenvironment ◽  
Single Cell ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cd8 T Cells ◽  
Nkt Cells ◽  
Ductal Adenocarcinoma ◽  
Hematopoietic Stem ◽  
Single Cell Sequencing ◽  
Prognostic Implications

Background: The treatment modalities for pancreatic ductal adenocarcinoma (PDAC) are limited and unsatisfactory. Although many novel drugs targeting the tumor microenvironment, such as immune checkpoint inhibitors, have shown promising efficacy for some tumors, few of them significantly prolong the survival of patients with PDAC due to insufficient knowledge on the tumor microenvironment.Methods: A single-cell RNA sequencing (scRNA-seq) dataset and seven PDAC cohorts with complete clinical and bulk sequencing data were collected for bioinformatics analysis. The relative proportions of each cell type were estimated using the gene set variation analysis (GSVA) algorithm based on the signatures identified by scRNA-seq or previous literature.Results: A meta-analysis of 883 PDAC patients showed that neutrophils are associated with worse overall survival (OS) for PDAC, while CD8+ T cells, CD4+ T cells, and B cells are related to prolonged OS for PDAC, with marginal statistical significance. Seventeen cell categories were identified by clustering analysis based on single-cell sequencing. Among them, CD8+ T cells and NKT cells were universally exhausted by expressing exhaustion-associated molecular markers. Interestingly, signatures of CD8+ T cells and NKT cells predicted prolonged OS for PDAC only in the presence of “targets” for pyroptosis and ferroptosis induction. Moreover, a specific state of T cells with overexpression of ribosome-related proteins was associated with a good prognosis. In addition, the hematopoietic stem cell (HSC)-like signature predicted prolonged OS in PDAC. Weighted gene co-expression network analysis identified 5 hub genes whose downregulation may mediate the observed survival benefits of the HSC-like signature. Moreover, trajectory analysis revealed that myeloid cells evolutionarily consisted of 7 states, and antigen-presenting molecules and complement-associated genes were lost along the pseudotime flow. Consensus clustering based on the differentially expressed genes between two states harboring the longest pseudotime span identified two PDAC groups with prognostic differences, and more infiltrated immune cells and activated immune signatures may account for the survival benefits.Conclusion: This study systematically investigated the prognostic implications of the components of the PDAC tumor microenvironment by integrating single-cell sequencing and bulk sequencing, and future studies are expected to develop novel targeted agents for PDAC treatment.

Fecal IgA Levels and Gut Microbiota Composition Are Regulated by Invariant Natural Killer T Cells

2019 ◽  
Vol 26 (5) ◽  
pp. 697-708 ◽  
Author(s):  
Cristhiane Favero de Aguiar ◽  
Angela Castoldi ◽  
Mariane T Amano ◽  
Aline Ignacio ◽  
Fernanda Fernandes Terra ◽  
...  
Keyword(s):  
T Cells ◽  
Gut Microbiota ◽  
Natural Killer ◽  
Natural Killer T Cells ◽  
Nkt Cells ◽  
Microbiota Composition ◽  
Inkt Cells ◽  
Intestinal Homeostasis ◽  
Killer T Cells ◽  
Gut Microbiota Composition

Abstract Background The gut microbiota is a key element to support host homeostasis and the development of the immune system. The relationship between the microbiota and immunity is a 2-way road, in which the microbiota contributes to the development/function of immune cells and immunity can affect the composition of microbes. In this context, natural killer T cells (NKT cells) are distinct T lymphocytes that play a role in gut immunity and are influenced by gut microbes. In our work, we investigated the involvement of invariant NKT cells (iNKT) in intestinal homeostasis. Results We found that iNKT-deficient mice (iNKT-KO) had reduced levels of fecal IgA and an altered composition of the gut microbiota, with increased Bacteroidetes. The absence of iNKT cells also affected TGF-β1 levels and plasma cells, which were significantly reduced in knockout (KO) mice. In addition, when submitted to dextran sodium sulfate colitis, iNKT-KO mice had worsening of colitis when compared with wild-type (WT) mice. To further address iNKT cell contribution to intestinal homeostasis, we adoptively transferred iNKT cells to KO mice, and they were submitted to colitis. Transfer of iNKT cells improved colitis and restored fecal IgA levels and gut microbiota. Conclusions Our results indicate that intestinal NKT cells are important modulators of intestinal homeostasis and that gut microbiota composition may be a potential target in the management of inflammatory bowel diseases.

scholarly journals Identification of Previously Unrecognized CD1d-Restricted Peripheral T Cell Lymphomas (PTCLs) in Mouse and Human Reveals Blocking Anti-CD1d Monoclonal Antibodies As a New Therapeutic Possibility in PTCLs

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4485-4485
Author(s):  
Emmanuel Bachy ◽  
Mirjam Urb ◽  
Gabriel Bricard ◽  
Shilpi Jayaswal ◽  
Remy Robinot ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Profile Analysis ◽  
Nkt Cells ◽  
Type I ◽  
Type Ii ◽  
Cell Of Origin ◽  
Gamma Delta ◽  
Inkt Cells ◽  
T Cell Lymphomas

Abstract Background. Peripheral T-cell lymphomas (PTCLs) originate from post-thymic T cells but compared to B-cell lymphomas the exact cell of origin is usually unknown except for angioimmunoblastic T-cell lymphoma arising from a follicular helper T-cell. Furthermore, no recurrent cytogenetic or molecular abnormalities are identified in PTCLs. Recently, recurrent impairment of the p53 pathway has been pointed out in PTCLs. However, p53 knockout (KO) mice are known to develop immature thymic T-cell lymphomas and solid tumors but surprisingly PTCLs have not been reported for more than 20 years in those mice. NKT cells are a T-cell subset responsive to glycolipids presented by CD1d, a major histocompatibility complex (MHC) class I-like antigen-presenting molecule, in contrast to conventional T cells, which recognize peptide antigens. Two types of NKT cells have been described so far: type I or invariant NKT cells (iNKT) that express a Valpha14-Jalpha18 (in mice) or Valpha24-Jalpha18 (in humans) constant chain and type II NKT cells that express a variable TCR but are CD1d-dependent as well. Most type II NKT cells are of alpha/beta phenotype but CD1d-restricted gamma/delta T cells have also been described in mice and humans. Methods. The development of PTCLs in p53 KO mice (B6.129S2-Trp53tm1Tyj/J) was studied. Identification of PTCLs was made by immunohistochemistry and flow cytometry analysis. Gene expression profile analysis (GeneChip Mouse Genome 430 2.0 array, Affymetrix) was performed to characterize lymphomas developed in the mouse model. Transfer experiments were done by intravenously retro-orbital injection into syngeneic, immunocompetent C57Bl/6J WT animals or immunocompromised CD3ε-/- mice. Therapeutic trials in mice were performed with the use of blocking anti-CD1d monoclonal antibodies (mAb) (clone HB323; BioXcell). Results. We found that p53 KO mice developed well-known and characterized thymic T-cell lymphomas and solid tumors as previously described. However, about 20% of p53 KO mice spontaneously developed a previously unrecognized entity of PTCLs originating from CD1d-restricted iNKT cells (ie type I NKT cells) referred to as NKTLs for NKT lymphomas thereafter. Both alpha-galactosylceramide-CD1d tetramer staining and unique Valpha14-Jalpha18 TCR rearrangement confirmed the iNKT nature of these lymphomas. Chronic injection of Streptococcus pneumoniae (Spn), reported to express glycolipid antigens activating NKT cells, significantly increased the incidence of these NKTLs compared to a control group of p53 KO mice injected with PBS (P=0.03). Gene expression profile analysis indicated a significant down-regulation of genes in the TCR signaling pathway of NKTLs (false discovery rate q-value=0.01 by gene set enrichment analysis) suggesting an underlying antigenic chronic stimulation as previously reported in chronically activated T cells (Figure 1). Moreover, NKTLs were characterized by upregulation of PD-1 and loss of NK1.1 expression compared to resting NKT cells (P<0.01 for both), which are features of activated and anergic iNKT cells. Altogether, those data indicate that NKTLs in mice could arise from chronically activated iNKT cells by endogenous or exogenous glycolipids. Furthermore, in vivo TCR/CD1d interactions were required for NKTLs survival after transfer in recipient mice and the use of blocking anti-CD1d mAb significantly prolonged mice overall survival (logrank P<0.001, Figure 2). We did not identify human PTCLs arising from type I iNKT cells by using alphaGalCer-CD1d tetramer staining. However, using sulfatide-loaded CD1d tetramers (ie another type of glycolipid-CD1d tetramer identifying type II NKT cells), we identified CD1d-restricted human PTCLs among gamma/delta hepatosplenic T-cell lymphomas (HSTLs) and PTCL-not otherwise specified (PTCL-NOS) expressing the Vd1 TCR but not the Vd2 TCR (Figure 3). Conclusion. This demonstrates for the first time the existence of human PTCLs arising from gamma/delta CD1d-restricted type II NKT cells. These results refine the classification of PTCLs in humans by identifying a new cell of origin and pave the way for the development of blocking anti-CD1d antibodies for therapeutic purposes. Figure 1. Figure 1. Figure 2. Figure 2. Figure 3. Figure 3. Disclosures No relevant conflicts of interest to declare.

scholarly journals CD1d-restricted Human Natural Killer T Cells Are Highly Susceptible to Human Immunodeficiency Virus 1 Infection

2002 ◽  
Vol 195 (7) ◽  
pp. 869-879 ◽  
Author(s):  
Alison Motsinger ◽  
David W. Haas ◽  
Aleksandar K. Stanic ◽  
Luc Van Kaer ◽  
Sebastian Joyce ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Natural Killer ◽  
Cell Receptor ◽  
Nkt Cells ◽  
Immunodeficiency Virus ◽  
Nk T Cells ◽  
Killer T Cells ◽  
Hiv 1

Human natural killer (NK) T cells are unique T lymphocytes that express an invariant T cell receptor (TCR) Vα24-Vβ11 and have been implicated to play a role in various diseases. A subset of NKT cells express CD4 and hence are potential targets for human immunodeficiency virus (HIV)-1 infection. We demonstrate that both resting and activated human Vα24+ T cells express high levels of the HIV-1 coreceptors CCR5 and Bonzo (CXCR6), but low levels of CCR7, as compared with conventional T cells. Remarkably NKT cells activated with α-galactosylceramide (α-GalCer)-pulsed dendritic cells were profoundly more susceptible to infection with R5-tropic, but not X4-tropic, strains of HIV-1, compared with conventional CD4+ T cells. Furthermore, resting CD4+ NKT cells were also more susceptible to infection. After initial infection, HIV-1 rapidly replicated and depleted the CD4+ subset of NKT cells. In addition, peripheral blood NKT cells were markedly and selectively depleted in HIV-1 infected individuals. Although the mechanisms of this decline are not clear, low numbers or absence of NKT cells may affect the course of HIV-1 infection. Taken together, our findings indicate that CD4+ NKT cells are directly targeted by HIV-1 and may have a potential role during viral transmission and spread in vivo.

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