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10.1128/JVI.00530-21 http://scihub22266oqcxt.onion/10.1128/JVI.00530-21 33952647!8274608!33952647     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33952647&cmd=llinks): Failed to open stream: HTTP request failed! 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CCR2 Regulates Vaccine-Induced Mucosal T-Cell Memory to Influenza A Virus |pdf=|usr=}}{{33952647}} gab.com Text CCR2 Regulates Vaccine-Induced Mucosal T-Cell Memory to Influenza A Virus JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=33952647 #FOAvip Elicitation of lung tissue-resident memory CD8 T cells (T(RM)s) is a goal of T cell-based vaccines against respiratory viral pathogens, such as influenza A virus (IAV). C-C chemokine receptor type 2 (CCR2)-dependent monocyte trafficking plays an essential role in the establishment of CD8 T(RM)s in lungs of IAV-infected mice. Here, we used a combination adjuvant-based subunit vaccine strategy that evokes multifaceted (T(C)1/T(C)17/T(H)1/T(H)17) IAV nucleoprotein-specific lung T(RM)s to determine whether CCR2 and monocyte infiltration are essential for vaccine-induced T(RM) development and protective immunity to IAV in lungs. Following intranasal vaccination, neutrophils, monocytes, conventional dendritic cells (DCs), and monocyte-derived dendritic cells internalized and processed vaccine antigen in lungs. We found that basic leucine zipper ATF-like transcription factor 3 (BATF3)-dependent DCs were essential for eliciting T cell responses, but CCR2 deficiency enhanced the differentiation of CD127(hi), KLRG-1(lo), OX40(+ve) CD62L(+ve), and mucosally imprinted CD69(+ve) CD103(+ve) effector and memory CD8 T cells in lungs and airways of vaccinated mice. Mechanistically, increased development of lung T(RM)s induced by CCR2 deficiency was linked to dampened expression of T-bet but not altered TCF-1 levels or T cell receptor signaling in CD8 T cells. T1/T17 functional programming, parenchymal localization of CD8/CD4 effector and memory T cells, recall T cell responses, and protective immunity to a lethal IAV infection were unaffected in CCR2-deficient mice. Taken together, we identified a negative regulatory role for CCR2 and monocyte trafficking in mucosal imprinting and differentiation of vaccine-induced T(RM)s. Mechanistic insights from this study may aid the development of T-cell-based vaccines against respiratory viral pathogens, including IAV and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). IMPORTANCE While antibody-based immunity to influenza A virus (IAV) is type and subtype specific, lung- and airway-resident memory T cells that recognize conserved epitopes in the internal viral proteins are known to provide heterosubtypic immunity. Hence, broadly protective IAV vaccines need to elicit robust T cell memory in the respiratory tract. We have developed a combination adjuvant-based IAV nucleoprotein vaccine that elicits strong CD4 and CD8 T cell memory in lungs and protects against H1N1 and H5N1 strains of IAV. In this study, we examined the mechanisms that control vaccine-induced protective memory T cells in the respiratory tract. We found that trafficking of monocytes into lungs might limit the development of antiviral lung-resident memory T cells following intranasal vaccination. These findings suggest that strategies that limit monocyte infiltration can potentiate vaccine-induced frontline T-cell immunity to respiratory viruses, such as IAV and SARS-CoV-2. Twit Text FOAVip CCR2 Regulates Vaccine-Induced Mucosal T-Cell Memory to Influenza A Virus ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=33952647 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33952647 #FOAvip English Wikipedia <ref>{{Cite pmid|33952647}}</ref> CCR2 Regulates Vaccine-Induced Mucosal T-Cell Memory to Influenza A Virus #MMPMID33952647 Lee W; Kingstad-Bakke B; Kedl RM; Kawaoka Y; Suresh M J Virol 2021[Jul]; 95 (15): e0053021 PMID33952647show ga Elicitation of lung tissue-resident memory CD8 T cells (T(RM)s) is a goal of T cell-based vaccines against respiratory viral pathogens, such as influenza A virus (IAV). C-C chemokine receptor type 2 (CCR2)-dependent monocyte trafficking plays an essential role in the establishment of CD8 T(RM)s in lungs of IAV-infected mice. Here, we used a combination adjuvant-based subunit vaccine strategy that evokes multifaceted (T(C)1/T(C)17/T(H)1/T(H)17) IAV nucleoprotein-specific lung T(RM)s to determine whether CCR2 and monocyte infiltration are essential for vaccine-induced T(RM) development and protective immunity to IAV in lungs. Following intranasal vaccination, neutrophils, monocytes, conventional dendritic cells (DCs), and monocyte-derived dendritic cells internalized and processed vaccine antigen in lungs. We found that basic leucine zipper ATF-like transcription factor 3 (BATF3)-dependent DCs were essential for eliciting T cell responses, but CCR2 deficiency enhanced the differentiation of CD127(hi), KLRG-1(lo), OX40(+ve) CD62L(+ve), and mucosally imprinted CD69(+ve) CD103(+ve) effector and memory CD8 T cells in lungs and airways of vaccinated mice. Mechanistically, increased development of lung T(RM)s induced by CCR2 deficiency was linked to dampened expression of T-bet but not altered TCF-1 levels or T cell receptor signaling in CD8 T cells. T1/T17 functional programming, parenchymal localization of CD8/CD4 effector and memory T cells, recall T cell responses, and protective immunity to a lethal IAV infection were unaffected in CCR2-deficient mice. Taken together, we identified a negative regulatory role for CCR2 and monocyte trafficking in mucosal imprinting and differentiation of vaccine-induced T(RM)s. Mechanistic insights from this study may aid the development of T-cell-based vaccines against respiratory viral pathogens, including IAV and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). IMPORTANCE While antibody-based immunity to influenza A virus (IAV) is type and subtype specific, lung- and airway-resident memory T cells that recognize conserved epitopes in the internal viral proteins are known to provide heterosubtypic immunity. Hence, broadly protective IAV vaccines need to elicit robust T cell memory in the respiratory tract. We have developed a combination adjuvant-based IAV nucleoprotein vaccine that elicits strong CD4 and CD8 T cell memory in lungs and protects against H1N1 and H5N1 strains of IAV. In this study, we examined the mechanisms that control vaccine-induced protective memory T cells in the respiratory tract. We found that trafficking of monocytes into lungs might limit the development of antiviral lung-resident memory T cells following intranasal vaccination. These findings suggest that strategies that limit monocyte infiltration can potentiate vaccine-induced frontline T-cell immunity to respiratory viruses, such as IAV and SARS-CoV-2. |*Immunity, Mucosal[MESH] |*Immunologic Memory[MESH] |Animals[MESH] |CD8-Positive T-Lymphocytes/*immunology[MESH] |Influenza A virus/genetics/*immunology[MESH] |Influenza Vaccines/genetics/*immunology/pharmacology[MESH] |Lung/immunology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Orthomyxoviridae Infections/genetics/*immunology/prevention & control[MESH] |Receptors, CCR2/genetics/*immunology[MESH]CCR2 Regulates Vaccine-Induced Mucosal T-Cell Memory to Influenza A Vi(epmc).pdf DeepDyve Pubget Overpricing