Inserted H–2 gene membrane products mediate immune response phenotype of antigen-presenting cell

Nature ◽  
1981 ◽  
Vol 291 (5817) ◽  
pp. 666-668 ◽  
Author(s):  
Aya Jakobovits ◽  
Ayala Frenkel ◽  
Nathan Sharon ◽  
Irun R. Cohen
Keyword(s):  
Immune Response ◽  
Antigen Presenting Cell ◽  
Mediate Immune Response ◽  
Response Phenotype ◽  
Antigen Presenting

scholarly journals Pros and Cons of Antigen-Presenting Cell Targeted Tumor Vaccines

2015 ◽  
Vol 2015 ◽  
pp. 1-18 ◽  
Author(s):  
Cleo Goyvaerts ◽  
Karine Breckpot
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Potential Benefit ◽  
Tumor Vaccines ◽  
Antigen Presenting Cell ◽  
Leading Role ◽  
True Meaning ◽  
Pros And Cons ◽  
Antigen Presenting

In therapeutic antitumor vaccination, dendritic cells play the leading role since they decide if, how, when, and where a potent antitumor immune response will take place. Since the disentanglement of the complexity and merit of different antigen-presenting cell subtypes, antitumor immunotherapeutic research started to investigate the potential benefit of targeting these subtypesin situ. This review will discuss which antigen-presenting cell subtypes are at play and how they have been targeted and finally question the true meaning of targeting antitumor-based vaccines.

scholarly journals Development of a Secondary Immune Response toMycobacterium tuberculosisIs Independent of Toll-Like Receptor 2

2010 ◽  
Vol 79 (3) ◽  
pp. 1118-1123 ◽  
Author(s):  
Amanda McBride ◽  
Kamlesh Bhatt ◽  
Padmini Salgame
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Host Resistance ◽  
Toll Like Receptor ◽  
Response Phenotype ◽  
Toll Like Receptor 2 ◽  
Antigen Presenting ◽  
Memory Immune Response

ABSTRACTPublished work indicates that the contribution of Toll-like receptor 2 (TLR2) to host resistance during acuteMycobacterium tuberculosisinfection is marginal. However, in these studies, TLR2 participation in the memory immune response toM. tuberculosiswas not determined. The substantialin vitroevidence thatM. tuberculosisstrongly triggers TLR2 on dendritic cells and macrophages to bring about either activation or inhibition of antigen-presenting cell (APC) functions, along with accumulating evidence that memory T cell development can be calibrated by TLR signals, led us to question the role of TLR2 in host resistance to secondary challenge withM. tuberculosis. To address this question, a memory immunity model was employed, and the response of TLR2-deficient (TLR2 knockout [TLR2KO]) mice following a secondary exposure toM. tuberculosiswas compared to that of wild-type (WT) mice based on assessment of the bacterial burden, recall response, phenotype of recruited T cells, and granulomatous response. We found that upon rechallenge withM. tuberculosis, both WT and TLR2KO immune mice displayed similarly enhanced resistance to infection in comparison to their naïve counterparts. The frequencies ofM. tuberculosis-specific gamma interferon (IFN-γ)-producing T cells, the phenotypes of recruited T cells, and the granulomatous responses were also similar between WT and TLR2KO immune mice. Together, the findings from this study indicate that TLR2 signaling does not influence memory immunity toM. tuberculosis.

Induction of an Immune Response for Imaging Antigen-Presenting Cell/T-Cell Interactions

2011 ◽  
Vol 2011 (2) ◽  
pp. pdb.prot5566-pdb.prot5566
Author(s):  
M. P. Matheu ◽  
M. D. Cahalan ◽  
I. Parker
Keyword(s):  
Immune Response ◽  
T Cell ◽  
Cell Interactions ◽  
Antigen Presenting Cell ◽  
Antigen Presenting

scholarly journals CD4+ Th1 Cells Induced by Dendritic Cell-Based Immunotherapy in Mice Chronically Infected with Leishmania amazonensis Do Not Promote Healing

2004 ◽  
Vol 72 (8) ◽  
pp. 4455-4463 ◽  
Author(s):  
Yannick F. Vanloubbeeck ◽  
Amanda E. Ramer ◽  
Fei Jie ◽  
Douglas E. Jones
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Leishmania Amazonensis ◽  
Interleukin 12 ◽  
Mrna Levels ◽  
Antigen Presenting Cell ◽  
Th1 Response ◽  
Ifn Γ ◽  
Antigen Presenting

ABSTRACT The susceptibility of mice to Leishmania amazonensis infection is thought to result from an inability to develop a Th1 response. Our data show that the low levels of gamma interferon (IFN-γ) produced by the draining lymph node (DLN) cells of chronically infected mice could be enhanced in vitro and in vivo with L. amazonensis antigen-pulsed bone marrow-derived dendritic cells (BM-DC) and the Th1-promoting cytokine interleukin-12 (IL-12). Given intralesionally to chronically infected mice, this treatment induced the upregulation of mRNA levels for IFN-γ, the transcription factor T-box expressed in T cells, and IL-12 receptor β2 in CD4+ T cells from the DLN and an increase in parasite-specific immunoglobulin G2a in the serum. However, this Th1 response was not associated with healing, and the antigen-specific enhancement of IFN-γ production remained impaired in the DLN. However, addition of IL-12 to the in vitro recall response was able to recover this defect, suggesting that antigen-presenting cell-derived IL-12 production may be limited in infected mice. This was supported by the fact that L. amazonensis amastigotes limited the production of IL-12p40 from BM-DC in vitro. Altogether, our data indicate that the immune response of mice chronically infected with L. amazonensis can be enhanced towards a Th1 phenotype but that the presence of Th1 CD4+ T cells does not promote healing. This suggests that the phenotype of the CD4+ T cells may not always be indicative of protection to L. amazonensis infection. Furthermore, our data support growing evidence that antigen-presenting cell function, such as IL-12 production, may limit the immune response in L. amazonensis-infected mice.

scholarly journals Gene complementation in the T-lymphocyte proliferative response to poly (Glu55Lys36Phe9)n. A demonstration that both immune response gene products must be expressed in the same antigen-presenting cell.

1979 ◽  
Vol 149 (1) ◽  
pp. 40-57 ◽  
Author(s):  
R H Schwartz ◽  
A Yano ◽  
J H Stimpfling ◽  
W E Paul
Keyword(s):  
Immune Response ◽  
T Lymphocyte ◽  
Parental Cell ◽  
Gene Products ◽  
Cell Type ◽  
Spleen Cells ◽  
Antigen Presenting Cell ◽  
Alpha Beta ◽  
Antigen Presenting ◽  
Ir Genes

The immune response (Ir) to the random copolymer GLphi depends upon the function of two Ir genes, Ir-GLphi-beta[beta] and Ir-GLphi-alpha[alpha], mapped to the I-A and I-E/C subregions of the major histocompatibility complex, respectively. In this paper, the site(s) of expression of the products of these two Ir genes was examined by evaluating T-lymphocyte proliferative responses of bone marrow radiation chimeras. Chimeras were created in [alpha+beta- X alpha-beta+]F1 responder mice by lethal irradiation and reconstitution with a mixture of bone marrow cells from both parental strains. These chimeras failed to respond to GLphi, although they were capable or responding to the much weaker antigens, (T,G)-A--L, TEPC-15, pigeon cytochrome c, and (H,G)-A--L. This failure to respond to GLphi was shown not to be the result of a cryptic mixed lymphocyte reaction, as similar chimeras created in (alpha+beta+ X alpha-beta+)F1 mice responded well to GLphi, although they possessed almost the same potential histoincompatibility. Furthermore, the lack of response to GLphi could not be attributed to a general failure of the two parental cell types in the chimeras to collaboratc with each other, as each chimeric parental cell type could respond to dinitrophenyl conjugated ovalbumin presented on nonimmune spleen cells from the other parent. Thus, the failure of low responder parental into F1 high responder chimeras to generate an immune response to GLphi suggests that immune competence for this antigen requires at least one cell type in the immune system to express gene products of both the Ir-glphi-alpha and -beta genes, i.e. one cell must be of high responder genotype. The the antigen-presenting cell is one such cell type was shown by experiments in which GLphi-primed T lymphocytes from responder F1 mice were stimulated with antigen bound to nonimmune spleen cells. Only spleen cells from responder F1 and recombinant mice could present GLphi. Neither of the two complementing nonresponder parental spleen cell populations, either alone or mixed together, could present GLphi, although both could present purified protein derivative of tuberculin. This was shown to be the case for T cells positively selected in vitro as well as freshly explanted T cells. Thus, both Ir-GLphi-alpha and Ir-GLphi-beta gene products must be expressed in the same antigen-presenting cell to generate a T-lymphocyte proliferative response to GLphi. The implications of these findings for models of two gene complementation are discussed.

scholarly journals Anatomical and Cellular Requirements for the Activation and Migration of Virus-Specific CD8+ T Cells to the Brain during Theiler's Virus Infection

2005 ◽  
Vol 79 (5) ◽  
pp. 3063-3070 ◽  
Author(s):  
Yanice V. Mendez-Fernandez ◽  
Michael J. Hansen ◽  
Moses Rodriguez ◽  
Larry R. Pease
Keyword(s):  
Bone Marrow ◽  
Immune Response ◽  
T Cells ◽  
T Cell ◽  
Cell Response ◽  
T Cell Response ◽  
Lymphoid Organs ◽  
Antigen Presenting Cell ◽  
Antigen Presenting ◽  
The Brain

ABSTRACT Theiler's murine encephalomyelitis virus (TMEV) infection of the brain induces a virus-specific CD8+ T-cell response in genetically resistant mice. The peak of the immune response to the virus occurs 7 days after infection, with an immunodominant CD8+ T-cell response against a VP2-derived capsid peptide in the context of the Db molecule. The process of activation of antigen-specific T cells that migrate to the brain in the TMEV model has not been defined. The site of antigenic challenge in the TMEV model is directly into the brain parenchyma, a site that is considered immune privileged. We investigated the hypothesis that antiviral CD8+ T-cell responses are initiated in situ upon intracranial inoculation with TMEV. To determine whether a brain parenchymal antigen-presenting cell is responsible for the activation of virus-specific CD8+ T cells, we evaluated the CD8+ T-cell response to the VP2 peptide in bone marrow chimeras and mutant mice lacking peripheral lymphoid organs. The generation of the anti-TMEV CD8+ T-cell response in the brain requires priming by a bone marrow-derived antigen-presenting cell and the presence of peripheral lymphoid organs. Although our results show that activation of TMEV-specific CD8+ T cells occurs in the peripheral lymphoid compartment, they do not exclude the possibility that the immune response to TMEV is initiated by a brain-resident, bone marrow-derived, antigen-presenting cell.

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