Humoral and T cell–mediated immune response against trichomoniasis

Abstract

Trichomonas vaginalis (T. vaginalis) infection leads to the synthesis of specific antibodies in the serum and local secretions. The profile of T. vaginalis-specific antibodies and T cell-mediated immune responses may influence the outcome of infection, towards parasite elimination, persistence or pathological reactions. Studies have indicated that Th1-, Th17- and Th22 cell-related cytokines may be protective or pathogenic, whereas Th2- and Treg cell-related cytokines can exert anti-inflammatory effects during T. vaginalis infection. A number of T. vaginalis-related components such as lipophosphoglycan (TvLPG), α-actinin, migration inhibitory factor (TvMIF), pyruvate:ferredoxin oxidoreductase (PFO), legumain-1 (TvLEGU-1), adhesins and cysteine proteases lead to the induction of specific antibodies. T. vaginalis has acquired several strategies to evade the humoral immune responses such as degradation of immunoglobulins by cysteine proteases, antigenic variation and killing of antibody-producing B cells. The characterization of the T. vaginalis-specific antibodies to significant immunogenic molecules and formulation of strategies to promote their induction in vaginal mucosa may reveal their potential protective effects against trichomoniasis. In this review, we discuss the current understanding of antibody and T cell-mediated immune responses to T. vaginalis and highlight novel insights into the possible role of immune responses in protection against parasite.

Microbiota in vaginal health and pathogenesis of recurrent vulvovaginal infections: a critical review

“…Other than this, adhesins including AP51 and AP65 of T. vaginalis were also shown to serve as heme and haemoglobin binding proteins, validating their multifunctional role in T. vaginalis [144]. A part from this, iron up-regulated cysteine proteases help in evasion of host's immune responses by degrading its various components that includes, subclasses of host antibodies (IgG and IgA), C3 opsonin, secretary leukocyte protease inhibitor (SLPI), an antimicrobial peptide and B cells [142,145,146]. In addition to iron, zinc also plays an important role in regulation of T. vaginalis proteins.…”

Contribution of monocytes and macrophages to the local tissue inflammation and cytokine storm in COVID-19: Lessons from SARS and MERS, and potential therapeutic interventions

“…Following the Th subset paradigm and based on the cultures of macrophages and in tumors, these cells are categorized into two principle subtypes, including M1 macrophages, which secrete great quantities of proinflammatory cytokines (such as IFN-γ, TNF-α, IL-6, and IL-12), nitric oxide and reactive oxygen species (ROS), whereas M2 macrophages release large concentrations of anti-inflammatory cytokines such as IL-10, TGF-β and IL-1 receptor antagonist [41,42]. M2 macrophages may be more subcategorized to M2a, M2b and M2c types which are induced from non-polarized macrophages via stimulation with IL-4/ IL-13, immune complexes plus TLR agonists, and IL-10/TGF-β/glucocorticoids, respectively [43].…”

Microbiome Dependent Regulation of Tregs and Th17 Cells in Mucosa

“…Lactobacilli largely impact the susceptibility to T. vaginalis infection in women. Although mechanisms are still under investigation, there is precedence that Th17 cells and T regs can have protective and anti-inflammatory effects during T. vaginalis infection (196). During a vaginal herpes simplex virus-2 (HSV-2) infection, mice lacking T regs fail to timely accumulate HSV-2-specific CD4 T cells and control the infection.…”