Immune response against toxoplasmosis—some recent updates RH:Toxoplasma gondiiimmune response

Abstract

Aims Cytokines, soluble mediators of immunity, are key factors of the innate and adaptive immune system. They are secreted from and interact with various types of immune cells to manipulate host body’s immune cell physiology for a counter-attack on the foreign body. A study was designed to explore the mechanism of Toxoplasma gondii ( T. gondii) resistance from host immune response. Methods and results The published data on aspect of host (murine and human) immune response against T. gondii was taken from Google scholar and PubMed. Most relevant literature was included in this study. The basic mechanism of immune response starts from the interactions of antigens with host immune cells to trigger the production of cytokines (pro-inflammatory and anti-inflammatory) which then act by forming a cytokinome (network of cytokine). Their secretory equilibrium is essential for endowing resistance to the host against infectious diseases, particularly toxoplasmosis. A narrow balance lying between Th1, Th2, and Th17 cytokines (as demonstrated until now) is essential for the development of resistance against T. gondii as well as for the survival of host. Excessive production of pro-inflammatory cytokines leads to tissue damage resulting in the production of anti-inflammatory cytokines which enhances the proliferation of Toxoplasma. Stress and other infectious diseases (human immunodeficiency virus (HIV)) that weaken the host immunity particularly the cellular component, make the host susceptible to toxoplasmosis especially in pregnant women. Conclusion The current review findings state that in vitro harvesting of IL12 from DCs, Np and MΦ upon exposure with T. gondii might be a source for therapeutic use in toxoplasmosis. Current review also suggests that therapeutic interventions leading to up-regulation/supplementation of SOCS-3, IL12, and IFNγ to the infected host could be a solution to sterile immunity against T. gondii infection. This would be of interest particularly in patients passing through immunosuppression owing to any reason like the ones receiving anti-cancer therapy, the ones undergoing immunosuppressive therapy for graft/transplantation, the ones suffering from immunodeficiency virus (HIV) or having AIDS. Another imortant suggestion is to launch the efforts for a vaccine based on GRA6Nt or other similar antigens of T. gondii as a probable tool to destroy tissue cysts.

Recurrent ocular toxoplasmosis infection in a patient with a selective deficiency of NK T-cells and cytotoxic СD8+ T-cells associated with a genetic folate cycle deficiency

“…These findings are in agreement with the current ideas on the mechanisms of immune surveillance of T. gondii, with a subset of cytotoxic NK T-cells having been attributed a key role in an effector immune response to the opportunistic pathogen [13]. The results of at least three recent reviews of clinical studies on immune protection in human toxoplasmosis have demonstrated key importance of cytotoxic СD8+ and NK T-cells in the control over the latent Toxoplasma in the human body [14,15,16]. It was obvious that deficiency of NKT cells and cytotoxic СD8+ T cells and was the most likely cause of a critical impairment in immune surveillance of endogenous T. gondii and the development of T. gondiiinduced acute chorioretinitis.…”

The imbalance in the relationship between inflammatory and regulatory cytokines during gestational toxoplasmosis can be harmful to fetuses: A systematic review

“…T. gondii drives a classical Th1 response in an immunocompetent host leading a production of pro-inflammatory mediators, in which IFN-γ, TNF, IL-12, IL-18, IL-1β, nitric oxide, CCL2, CXCL2, CXCR3 and MyD88-dependenty factors, are critical for host survival ( 17 , 55 , 56 ). Indeed, this protective scenario is mediated by antigen-presenting cells (eg.…”

Tryptophan metabolism and immune alterations in pregnant Hispanic women with chronic Toxoplasma gondii infection

“…Our findings of reduced levels of certain Th‐1 and proinflammatory cytokines (IFN‐γ, IL‐17, IL‐12, IL‐6) either throughout pregnancy or at certain times during pregnancy suggest that T cell function in chronically infected pregnant women may be altered. Throughout the life of the chronically infected host there is an equilibrium between the parasite survival and the Th‐1, Th2, Th‐17, and T regulatory (Treg) host responses to the parasite 35 . Maintenance of quiescence involves a balance between pro‐ and anti‐inflammatory cytokines.…”