scholarly journals Effect of female sex steroids on splenocyte ability to produce an adoptive immune response. Role of prostaglandin F2a in hormonal immunoregulation mechanisms

1994 ◽  
Vol 40 (3) ◽  
pp. 47-49 ◽  
Author(s):  
S. V. Shirshev ◽  
Yu. I. Shilov ◽  
N. N. Kevorkov
Keyword(s):  
Cell Culture ◽  
Immune Response ◽  
T Lymphocytes ◽  
Sex Steroids ◽  
Negative Effects ◽  
Cba Mice ◽  
Prostaglandin F2a ◽  
Culture Supernatants ◽  
Stimulation Of

Male CBA mice were used in experiments. Splenocytes were incubated for an hour in macrocultures with estradiol (E2) or progesterone (P), then the cells were transferred (together with the antigen) to lethally irradiated syngeneic recipients, and on day 4 the count of antibody-producing cells (APC) was estimated. Prostaglandin F2a (PGF2a) concentrations were radioimmunoassayed in cell culture supernatants. E2 and P concentrations corresponded to these hormones levels in blood sera during pregnancy. E2 and P in the tested concentrations were found to reliably stimulate the processes of APC formation, their effects being dose independent. Both E2 and P statistically reliably increased PGF2a level in splenocyte culture. Fractionation of splenocytes helped reveal the highest PGF2a level in the cultures devoid of adhesive cells and rich for T lymphocytes. Hence, E2 and P stimulated the processes of antigen-independent differentiation of splenocytes producing APC either by directly stimulating T lymphocytes or via macrophages by blocking their negative effects. Stimulation of adoptive immune response by sex steroids is closely connected with PGF2a production by immunocompetent cells under the effects of these hormones.

The role of bacterial super antigens in the immune response: From biology to cancer treatment

2020 ◽  
Vol 16 ◽  
Author(s):  
Behnam Emamgolizadeh Gurt Tapeh ◽  
Mohammad Sadegh Hashemzadeh ◽  
Ali Mir Hoseini
Keyword(s):  
Immune Response ◽  
Immune System ◽  
T Lymphocytes ◽  
Cancer Treatment ◽  
Tumor Cells ◽  
Vector Systems ◽  
Bacterial Vector ◽  
Antigen Presenting ◽  
Stimulation Of

Aims: Encouraging results have been indicated preclinically and in patients using the bacterial super antigen. This review article intends to summarize the role of the super antigens that have been recently used in the treatment of cancer. In addition, the vector systems including lentiviral vectors, adeno-associated vector systems and retroviral vectors that are increasingly being used in basic and applied research were discussed. Most importantly, the new CRISPR technique has also been discussed in this literature review. Discussion: More successful therapies can be achieved by manipulating bacterial vector systems through incorporating genes related to the super antigens and cytokines. The products of SAg and cytokine genes contributes to the strong stimulation of immune system against tumor cells. They bind to MHC II molecules as well as the V beta regions of TCR and lead to the production of IL2 and other cytokines, the activation of antigen-presenting cells and T lymphocytes. Additionally, super antigens can be used to eradicate tumor cells. Better results in cancer treatment can be achieved by transferring super antigen genes and subsequent strong immune stimulation along with other cancer immunotherapy agents. Conclusion: Super antigens induce the proliferation of T lymphocytes and antigen-presenting cells by binding to MHCII molecules and V beta regions in T cell receptors. Therefore, the presentation of tumor cell antigens is increased. Additionally, the production of important cytokines by T cells and APCs contributes to the stimulation of immune response against tumor cells. The manipulation of bacterial vector systems through incorporating genes related to SAgs and other immune response factors is a good strategy for immune system stimulating and eradicating of tumor cells along with other immunotherapy agents.

scholarly journals Influenza virus-specific CD4+ T helper type 2 T lymphocytes do not promote recovery from experimental virus infection.

1994 ◽  
Vol 180 (4) ◽  
pp. 1273-1282 ◽  
Author(s):  
M B Graham ◽  
V L Braciale ◽  
T J Braciale
Keyword(s):  
Immune Response ◽  
T Cells ◽  
T Lymphocytes ◽  
Cd4 T Cells ◽  
Primary Role ◽  
T Helper ◽  
Helper Type

T lymphocytes play a primary role in recovery from viral infections and in antiviral immunity. Although viral-specific CD8+ and CD4+ T cells have been shown to be able to lyse virally infected targets in vitro and promote recovery from lethal infection in vivo, the role of CD4+ T lymphocytes and their mechanism(s) of action in viral immunity are not well understood. The ability to further dissect the role that CD4+ T cells play in the immune response to a number of pathogens has been greatly enhanced by evidence for more extensive heterogeneity among the CD4+ T lymphocytes. To further examine the role of CD4+ T cells in the immune response to influenza infection, we have generated influenza virus-specific CD4+ T cell clones from influenza-primed BALB/c mice with differential cytokine secretion profiles that are defined as T helper type 1 (Th1) clones by the production of interleukin 2 (IL-2) and interferon gamma (IFN-gamma), or as Th2 clones by the production of IL-4, IL-5, and IL-10. Our studies have revealed that Th1 clones are cytolytic in vitro and protective against lethal challenge with virus in vivo, whereas Th2 clones are noncytolytic and not protective. Upon further evaluation of these clonal populations we have shown that not only are the Th2 clones nonprotective, but that pulmonary pathology is exacerbated as compared with control mice as evidenced by delayed viral clearance and massive pulmonary eosinophilia. These data suggest that virus-specific CD4+ T cells of the Th2 subset may not play a primary role in virus clearance and recovery and may lead to immune mediated potentiation of injury.

On the Role of T Lymphocytes in Stimulation of Humoral Immunity Induced by Peptidoglycan–Monomer Linked with Zinc

1999 ◽  
Vol 119 (1) ◽  
pp. 13-22 ◽  
Author(s):  
Jagoda Ravlić-Gulan ◽  
Biserka Radošević-Stašić ◽  
Zlatko Trobonjača ◽  
Marija Petković ◽  
Mira Ćuk ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Humoral Immunity ◽  
Stimulation Of

The role of regulatory T lymphocytes in the induced immune response mediated by biological vaccines

Immunobiology ◽  
2006 ◽  
Vol 211 (1-2) ◽  
pp. 127-136 ◽  
Author(s):  
Mercedes López ◽  
Raquel Aguilera ◽  
Claudio Pérez ◽  
Ariadna Mendoza-Naranjo ◽  
Cristian Pereda ◽  
...  
Keyword(s):  
Immune Response ◽  
T Lymphocytes ◽  
Regulatory T Lymphocytes

scholarly journals Neutralization or Absence of the Interleukin-23 Pathway Does Not Compromise Immunity to Mycobacterial Infection

2006 ◽  
Vol 74 (11) ◽  
pp. 6092-6099 ◽  
Author(s):  
Alissa A. Chackerian ◽  
Shi-Juan Chen ◽  
Scott J. Brodie ◽  
Jeanine D. Mattson ◽  
Terrill K. McClanahan ◽  
...  
Keyword(s):  
Immune Response ◽  
Secondary Infection ◽  
Mycobacterial Infection ◽  
Effective Control ◽  
Bacterial Burden ◽  
Wild Type ◽  
Interleukin 23 ◽  
Deficient Mice ◽  
Stimulation Of

ABSTRACT Interleukin-23 (IL-23), a member of the IL-12 family, is a heterodimeric cytokine that is composed of the p40 subunit of IL-12 plus a unique p19 subunit. IL-23 is critical for autoimmune inflammation, in part due to its stimulation of the proinflammatory cytokine IL-17A. It is less clear, however, if IL-23 is required during the immune response to pathogens. We examined the role of IL-23 during Mycobacterium bovis BCG infection. We found that IL-23 reduces the bacterial burden and promotes granuloma formation when IL-12 is absent. However, IL-23 does not contribute substantially to host resistance when IL-12 is present, as the ability to control bacterial growth and form granulomata is not affected in IL-23p19-deficient mice and mice treated with a specific anti-IL-23p19 antibody. IL-23p19-deficient mice are also able to mount an effective memory response to secondary infection with BCG. While IL-23p19-deficient mice do not produce IL-17A, this cytokine is not necessary for effective control of infection, and antibody blocking of IL-17A in both wild-type and IL-12-deficient mice also has little effect on the bacterial burden. These data suggest that IL-23 by itself does not play an essential role in the protective immune response to BCG infection; however, the presence of IL-23 can partially compensate for the absence of IL-12. Furthermore, neutralization of IL-23 or IL-17A does not increase susceptibility to mycobacterial BCG infection.

scholarly journals FUNCTION OF MACROPHAGES IN ANTIGEN RECOGNITION BY GUINEA PIG T LYMPHOCYTES

1973 ◽  
Vol 138 (5) ◽  
pp. 1213-1229 ◽  
Author(s):  
Ethan M. Shevach ◽  
Alan S. Rosenthal
Keyword(s):  
Immune Response ◽  
T Cells ◽  
T Lymphocytes ◽  
Binding Site ◽  
T Lymphocyte ◽  
Lymphocyte Transformation ◽  
Antigen Recognition ◽  
Histocompatibility Antigens ◽  
Recognition Sites

A number of recent studies have suggested that the main functional role of the product of the immune response (Ir) genes is in the process of antigen recognition by the T lymphocyte. The observation in the accompanying report that the interaction of macrophage-associated antigen with immune T lymphocytes requires that both cells share histocompatibility antigens raised the question as to whether the macrophage played a role in the genetic control of the immune response or even if the macrophage were the primary cell in which the product of the Ir gene is expressed. In the current study, parental macrophages were pulsed with an antigen, the response to which is controlled by an Ir gene lacking in that parent; these macrophages were then mixed with T cells derived from the (nonresponder x responder)F1 and the resultant stimulation was measured. No stimulation was seen when column-purified F1 lymph node lymphocytes were mixed with antigen-pulsed macrophages from the nonresponder parent. However, when the highly reactive peritoneal exudate lymphocyte population was used as the indicator cells, parental macrophages pulsed with an antigen whose Ir gene they lacked were capable of initiating F1 T-cell proliferation. The magnitude of stimulation was approximately 1/10 that seen when macrophages from either the responder parent or the F1 were used. In order to explain this observation, we hypothesize that antigen recognition sites on the T lymphocyte are physically related to a macrophage-binding site and both are linked to the serologically determined histocompatibility antigens. Thus, parental macrophages pulsed with an antigen, whose Ir gene they lack, activate F1 cells poorly because the recognition sites for the antigen are physically related to the macrophage-binding site of the responder parent while the main contacts between the cells are at the nonresponder binding sites. Experiments performed with alloantisera lend support to this hypothesis. Thus, when parental macrophages are pulsed with any antigen and added to F1 T cells, an alloantiserum directed against parental histocompatibility antigens reacts with both the lymphocyte and the macrophage and thereby inhibits macrophage-lymphocyte interaction and abolishes antigen-induced lymphocyte transformation. When the alloantisera are directed at determinants present solely on the T lymphocyte, they only inhibit the recognition of antigens controlled by the Ir gene linked to the histocompatibility antigen against which they are directed. We conclude from these studies that antigen recognition by the T lymphocyte is a complex multicellular event involving more than simple antigen binding to a specific lymphocyte receptor.

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