scholarly journals Reduced T Cell–Dependent Humoral Immune Response in Microsomal Prostaglandin E Synthase-1 Null Mice Is Mediated by Nonhematopoietic Cells

2013 ◽  
Vol 191 (10) ◽  
pp. 4979-4988 ◽  
Author(s):  
Fumiaki Kojima ◽  
Andrey Frolov ◽  
Rahul Matnani ◽  
Jerold G. Woodward ◽  
Leslie J. Crofford
Keyword(s):  
Immune Response ◽  
T Cell ◽  
Humoral Immune Response ◽  
Prostaglandin E ◽  
Prostaglandin E Synthase ◽  
Humoral Immune ◽  
Microsomal Prostaglandin E Synthase

scholarly journals Association between Reactogenicity and Immunogenicity after Vaccination with BNT162b2

Vaccines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1089
Author(s):  
Stilla Bauernfeind ◽  
Bernd Salzberger ◽  
Florian Hitzenbichler ◽  
Karolina Scigala ◽  
Sebastian Einhauser ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cell ◽  
Immune Responses ◽  
Humoral Immune Response ◽  
Adverse Reactions ◽  
Medical Center ◽  
Neutralization Activity ◽  
Humoral Immune ◽  
Cell Mediated Immune Response ◽  
Severe Adverse Reactions

It is not clear whether there is an association between adverse reactions and immune response after vaccination. Seven hundred and thirty-five vaccinees from our University Medical Center vaccination clinic provided information about sex, age and adverse reactions after first and second vaccination with BNT162b2. Adverse reactions were categorized into three groups: no or minor on the injection side, moderate (not further classified) and severe—defined as any symptom(s) resulting in sick leave. We chose 38 vaccinees with the most severe adverse reactions and compared their humoral and T-cell-mediated immune responses after second vaccination with those of 38 sex and age matched controls without or only minor injection-side related adverse reactions. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) anti-receptor binding domain (RBD) IgG titers were detectable in all participants (median 5528; range 958–26,285). Men with severe adverse reactions had 1.5-fold higher median SARS-CoV-2 RBD IgG titers compared to men without adverse reactions (median 7406 versus 4793; p < 0.001). Similarly; neutralization activity was significantly higher in men with severe adverse reactions (half maximal inhibitory concentrations (IC50) median 769 versus 485; p < 0.001). Reactogenicity did not influence humoral immune response in women nor T-cell-mediated immune response in any sex. To conclude; adverse reactions after vaccination with BNT162b2 do influence humoral immune response yet only in men and are not a prerequisite for a robust antibody response.

scholarly journals Neonatally Induced Inactivation of the Vascular Cell Adhesion Molecule 1 Gene Impairs B Cell Localization and T Cell–Dependent Humoral Immune Response

2001 ◽  
Vol 193 (6) ◽  
pp. 755-768 ◽  
Author(s):  
Christoph E. Leuker ◽  
Mark Labow ◽  
Werner Müller ◽  
Norbert Wagner
Keyword(s):  
Immune Response ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Adhesion Molecule ◽  
Humoral Immune Response ◽  
Cellular Adhesion ◽  
Humoral Immune ◽  
Cell Localization ◽  
Cellular Adhesion Molecule

Vascular cellular adhesion molecule (VCAM)-1 is a membrane-bound cellular adhesion molecule that mediates adhesive interactions between hematopoietic progenitor cells and stromal cells in the bone marrow (BM) and between leukocytes and endothelial as well as dendritic cells. Since VCAM-1–deficient mice die embryonically, conditional VCAM-1 mutant mice were generated to analyze the in vivo function of this adhesion molecule. Here we show that interferon-induced Cre-loxP–mediated deletion of the VCAM-1 gene after birth efficiently ablates expression of VCAM-1 in most tissues like, for example, BM, lymphoid organs, and lung, but not in brain. Induced VCAM-1 deficiency leads to a reduction of immature B cells in the BM and to an increase of these cells in peripheral blood but not in lymphoid organs. Mature recirculating B cells are reduced in the BM. In a migration assay, the number of mature B cells that appears in the BM after intravenous injection is decreased. In addition, the humoral immune response to a T cell–dependent antigen is impaired. VCAM-1 serves an important role for B cell localization and the T cell–dependent humoral immune response.

scholarly journals B and CD4+ T-cell expression of TLR2 is critical for optimal induction of a T-cell-dependent humoral immune response to intact Streptococcus pneumoniae

2008 ◽  
Vol 38 (12) ◽  
pp. 3316-3326 ◽  
Author(s):  
Sam Vasilevsky ◽  
Gouri Chattopadhyay ◽  
Jesus Colino ◽  
Tze-Jou Yeh ◽  
Quanyi Chen ◽  
...  
Keyword(s):  
Immune Response ◽  
Streptococcus Pneumoniae ◽  
T Cell ◽  
Humoral Immune Response ◽  
Cd4 T Cell ◽  
Humoral Immune ◽  
Cell Expression

scholarly journals AJP001, a novel helper T‐cell epitope, induces a humoral immune response with activation of innate immunity when included in a peptide vaccine

2019 ◽  
Vol 1 (12) ◽  
pp. 760-772 ◽  
Author(s):  
Akiko Tenma ◽  
Hironori Nakagami ◽  
Hideki Tomioka ◽  
Makoto Sakaguchi ◽  
Ryoko Ide ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
T Cell ◽  
Humoral Immune Response ◽  
Peptide Vaccine ◽  
Cell Epitope ◽  
T Cell Epitope ◽  
Helper T Cell ◽  
Humoral Immune

scholarly journals T Cell-Derived Lymphotoxin Is Essential for the Anti-Herpes Simplex Virus 1 Humoral Immune Response

2018 ◽  
Vol 92 (14) ◽  
Author(s):  
Kaiting Yang ◽  
Yong Liang ◽  
Zhichen Sun ◽  
Diyuan Xue ◽  
Hairong Xu ◽  
...  
Keyword(s):  
Immune Response ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Humoral Immune Response ◽  
Herpes Simplex Virus 1 ◽  
Humoral Immune ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACTB cell-derived lymphotoxin (LT) is required for the development of follicular dendritic cell clusters for the formation of primary and secondary lymphoid follicles, but the role of T cell-derived LT in antibody response has not been well demonstrated. We observed that lymphotoxin β-receptor (LTβR) signaling is essential for optimal humoral immune response and protection against an acute herpes simplex virus 1 (HSV-1) infection. Blocking the LTβR pathway caused poor maintenance of germinal center B (GC-B) cells and follicular helper T (Tfh) cells. Using bone marrow chimeric mice and adoptive transplantation, we determined that T cell-derived LT played an indispensable role in the humoral immune response to HSV-1. Upregulation of gamma interferon by the LTβR-Ig blockade impairs the sustainability of Tfh-like cells, leading to an impaired humoral immune response. Our findings have identified a novel role of T cell-derived LT in the humoral immune response against HSV-1 infection.IMPORTANCEImmunocompromised people are susceptible to HSV-1 infection and lethal recurrence, which could be inhibited by anti-HSV-1 humoral immune response in the host. This study sought to explore the role of T cell-derived LT in the anti-HSV-1 humoral immune response using LT-LTβR signaling-deficient mice and the LTβR-Ig blockade. The data indicate that the T cell-derived LT may play an essential role in sustaining Tfh-like cells and ensure Tfh-like cells' migration into primary or secondary follicles for further maturation. This study provides insights for vaccine development against infectious diseases.

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