Mechanisms Underlying the Induction of Regulatory T cells and Its Relevance in the Adaptive Immune Response in Parasitic Infections

The current coronavirus disease 2019 (COVID-19) pandemic, a disease caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), was first identified in December 2019 in China, and has led to thousands of mortalities globally each day. While the innate immune response serves as the first line of defense, viral clearance requires activation of adaptive immunity, which employs B and T cells to provide sanitizing immunity. SARS-CoV-2 has a potent arsenal of mechanisms used to counter this adaptive immune response through processes, such as T cells depletion and T cell exhaustion. These phenomena are most often observed in severe SARS-CoV-2 patients, pointing towards a link between T cell function and disease severity. Moreover, neutralizing antibody titers and memory B cell responses may be short lived in many SARS-CoV-2 patients, potentially exposing these patients to re-infection. In this review, we discuss our current understanding of B and T cells immune responses and activity in SARS-CoV-2 pathogenesis.

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Engineered Antigen-Specific T Cells Secreting Broadly Neutralizing Antibodies: Combining Innate and Adaptive Immune Response against HIV

Molecular Therapy — Methods & Clinical Development ◽

10.1016/j.omtm.2020.08.015 ◽

2020 ◽

Vol 19 ◽

pp. 78-88

Author(s):

Allison B. Powell ◽

Yanqin Ren ◽

Maria Korom ◽

Devin Saunders ◽

Patrick J. Hanley ◽

...

Keyword(s):

Immune Response ◽

T Cells ◽

Neutralizing Antibodies ◽

Adaptive Immune Response ◽

Broadly Neutralizing Antibodies ◽

Adaptive Immune

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Reduced Immune Response to Borrelia burgdorferi in the Absence of γδ T Cells

Infection and Immunity ◽

10.1128/iai.00148-11 ◽

2011 ◽

Vol 79 (10) ◽

pp. 3940-3946 ◽

Cited By ~ 16

Author(s):

Cuixia Shi ◽

Bikash Sahay ◽

Jennifer Q. Russell ◽

Karen A. Fortner ◽

Nicholas Hardin ◽

...

Keyword(s):

Immune Response ◽

T Cells ◽

Borrelia Burgdorferi ◽

Adaptive Immune Response ◽

Γδ T Cells ◽

Content Type ◽

Adaptive Immune ◽

Cytokines And Chemokines

ABSTRACTLittle is known regarding the function of γδ T cells, although they accumulate at sites of inflammation in infections and autoimmune disorders. We previously observed that γδ T cellsin vitroare activated byBorrelia burgdorferiin a TLR2-dependent manner. We now observe that the activated γδ T cells can in turn stimulate dendritic cellsin vitroto produce cytokines and chemokines that are important for the adaptive immune response. This suggested thatin vivoγδ T cells may assist in activating the adaptive immune response. We examined this possibilityin vivoand observed that γδ T cells are activated and expand in number duringBorreliainfection, and this was reduced in the absence of TLR2. Furthermore, in the absence of γδ T cells, there was a significantly blunted response of adaptive immunity, as reflected in reduced expansion of T and B cells and reduced serum levels of anti-Borreliaantibodies, cytokines, and chemokines. This paralleled a greaterBorreliaburden in γδ-deficient mice as well as more cardiac inflammation. These findings are consistent with a model of γδ T cells functioning to promote the adaptive immune response during infection.

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Initiation of the adaptive immune response to Mycobacterium tuberculosis depends on antigen production in the local lymph node, not the lungs

Journal of Experimental Medicine ◽

10.1084/jem.20071367 ◽

2007 ◽

Vol 205 (1) ◽

pp. 105-115 ◽

Cited By ~ 344

Author(s):

Andrea J. Wolf ◽

Ludovic Desvignes ◽

Beth Linas ◽

Niaz Banaiee ◽

Toshiki Tamura ◽

...

Keyword(s):

Immune Response ◽

T Cells ◽

Mycobacterium Tuberculosis ◽

Lymph Node ◽

T Cell Activation ◽

Cd4 T Cells ◽

Adaptive Immune Response ◽

Adaptive Immune ◽

Initial Activation ◽

Local Lymph Node

The onset of the adaptive immune response to Mycobacterium tuberculosis is delayed compared with that of other infections or immunization, and allows the bacterial population in the lungs to expand markedly during the preimmune phase of infection. We used adoptive transfer of M. tuberculosis Ag85B-specific CD4+ T cells to determine that the delayed adaptive response is caused by a delay in initial activation of CD4+ T cells, which occurs earliest in the local lung-draining mediastinal lymph node. We also found that initial activation of Ag85B-specific T cells depends on production of antigen by bacteria in the lymph node, despite the presence of 100-fold more bacteria in the lungs. Although dendritic cells have been found to transport M. tuberculosis from the lungs to the local lymph node, airway administration of LPS did not accelerate transport of bacteria to the lymph node and did not accelerate activation of Ag85B-specific T cells. These results indicate that delayed initial activation of CD4+ T cells in tuberculosis is caused by the presence of the bacteria in a compartment that cannot be mobilized from the lungs to the lymph node, where initial T cell activation occurs.

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