Complement receptor 3 is required for maximum in vitro trogocytic killing of the parasite Trichomonas vaginalis by human neutrophil-like cells.

Trichomonas vaginalis (Tv) is a parasite that causes trichomoniasis, a prevalent sexually-transmitted infection. Neutrophils are found at the site of infection, and can rapidly kill the parasite in vitro, using trogocytosis. However, the specific molecular players in neutrophil killing of Tv are unknown.

Neutrophil-like cells derived from the HL-60 cell-line as a genetically-tractable model for neutrophil degranulation.

Research on neutrophil biology has been limited by the short life span and limited genetic manipulability of these cells, driving the need for representative and efficient model cell lines. The promyelocytic cell line HL-60 and its subline PLB-985 can be differentiated into neutrophil-like cells (NLCs) and have been used to study neutrophil functions including chemotaxis, phagocytosis, endocytosis, and degranulation. Compared to neutrophils derived from hematopoietic stem cells, NLCs serve as a cost-effective neutrophil model.

Bovine neutrophils kill the sexually-transmitted parasite Tritrichomonas foetus using trogocytosis.

The protozoan parasite Tritrichomonas foetus (T. foetus) is the causative organism of bovine trichomonosis (also referred to as trichomoniasis), a sexually-transmitted infection that reduces fertility in cattle. Efforts to control trichomonosis on cattle farms are hindered by the discouragement of antibiotic use in agriculture, and the incomplete, short-lived protection conferred by the current vaccines.

Trichomonas vaginalis adherence phenotypes and extracellular vesicles impact parasite survival in a novel in vivo model of pathogenesis.

Trichomonas vaginalis is a human infective parasite responsible for trichomoniasis-the most common, non-viral, sexually transmitted infection worldwide. T. vaginalis resides exclusively in the urogenital tract of both men and women.

Human neutrophil-like cells demonstrate antimicrobial responses to the chronic cyst form of Toxoplasma gondii.

The protozoan parasite Toxoplasma gondii infects approximately 2.5 billion people worldwide. Infection induces a rapid dissemination of parasites throughout the body followed by the formation of lifelong cysts within neurons of the host brain.

Neutrophil interactions with the sexually transmitted parasite implications for immunity and pathogenesis.

Trichomoniasis is the third most common sexually transmitted infection in humans and is caused by the protozoan parasite, (). Pathogenic outcomes are more common in women and generally include mild vaginitis or cervicitis. However, more serious effects associated with trichomoniasis include adverse reproductive outcomes.

Active Learning and Technology Approaches for Teaching Immunology to Undergraduate Students.

Immunology is a fascinating and extremely complex field, with natural connections to many disciplines both within STEM and beyond. Teaching an undergraduate course in immunology therefore provides both opportunities and challenges. Significant challenges to student learning include mastering the volume of new vocabulary and figuring out how to think coherently about a physiological system that is so anatomically disseminated.

Targeting the Achievement Gap: Strategies Toward Removing Inequities in Undergraduate Immunology Education.

A diverse student body enriches the classroom with lived experiences, varied skillsets, community and cultural knowledge, resiliency, and altruistic interests, all critical attributes that benefit both the classroom and the STEM field at large. However, a persistent disparity in academic and educational attainment exists between under-represented minority (URM) and non-URM students in STEM fields. This achievement gap discourages talented URM students from entering STEM professions, threatening the potential, expertise, and perspective of these professions.

Trichomonas vaginalis: Pathogenesis, Symbiont Interactions, and Host Cell Immune Responses.

The parasite Trichomonas vaginalis (Tv) causes a highly prevalent sexually transmitted infection. As an extracellular pathogen, the parasite mediates adherence to epithelial cells to colonize the human host. In addition, the parasite interfaces with the host immune system and the vaginal microbiota.

Neutrophils kill the parasite Trichomonas vaginalis using trogocytosis.

T. vaginalis, a human-infective parasite, causes the most common nonviral sexually transmitted infection (STI) worldwide and contributes to adverse inflammatory disorders. The immune response to T.

Leukocyte Lysis and Cytokine Induction by the Human Sexually Transmitted Parasite Trichomonas vaginalis.

Trichomonas vaginalis (Tv) is an extracellular protozoan parasite that causes the most common non-viral sexually transmitted infection: trichomoniasis. While acute symptoms in women may include vaginitis, infections are often asymptomatic, but can persist and are associated with medical complications including increased HIV susceptibility, infertility, pre-term labor, and higher incidence of cervical cancer. Heightened inflammation resulting from Tv infection could account for these complications.

Differentiation of IL-17-producing effector and regulatory human T cells from lineage-committed naive precursors.

A subset of human regulatory T cells (Tregs) secretes IL-17 and thus resembles Th17 effector cells. How IL-17(+) Tregs differentiate from naive precursors remains unclear. In this study, we show that IL-17-producing T cells can differentiate from CCR6(+) naive T cell precursors in the presence of IL-2, IL-1β, TGF-β, and IL-23.

Trichomonas vaginalis homolog of macrophage migration inhibitory factor induces prostate cell growth, invasiveness, and inflammatory responses.

The human-infective parasite Trichomonas vaginalis causes the most prevalent nonviral sexually transmitted infection worldwide. Infections in men may result in colonization of the prostate and are correlated with increased risk of aggressive prostate cancer. We have found that T.

The metalloprotease ADAM12 regulates the effector function of human Th17 cells.

A key modulator of immune homeostasis, TGFβ has an important role in the differentiation of regulatory T cells (Tregs) and IL-17-secreting T cells (Th17). How TGFβ regulates these functionally opposing T cell subsets is not well understood. We determined that an ADAM family metalloprotease called ADAM12 is specifically and highly expressed in both Tregs and CCR6+ Th17 cells.

Probing the effector and suppressive functions of human T cell subsets using antigen-specific engineered T cell receptors.

Activation of T cells through the engagement of the T cell receptors (TCRs) with specific peptide-MHC complexes on antigen presenting cells (APCs) is the major determinant for their proliferation, differentiation and display of effector functions. To assess the role of quantity and quality of peptide-MHC presentation in eliciting T cell activation and suppression functions, we genetically engineered human T cells with two TCRs that recognize HLA-A*0201-restricted peptides derived from either HIV or melanoma antigens. The engineered-TCRs are highly functional in both CD8(+) and CD4(+) T cells as assessed by the upregulation of activation markers, induction of cytokine secretion and cytotoxicity.

Expression and function of TNF and IL-1 receptors on human regulatory T cells.

Regulatory T cells (Tregs) suppress immune activation and are critical in preventing autoimmune diseases. While the ability of Tregs to inhibit proliferation of other T cells is well established, it is not yet clear whether Tregs also modulate inflammatory cytokines during an immune response. Here, we show that the expression of inflammatory cytokine receptors IL-1R1 and TNFR2 were higher on resting mature Tregs compared to naïve or memory T cells.

Expression of GARP selectively identifies activated human FOXP3+ regulatory T cells.

The molecules that define human regulatory T cells (Tregs) phenotypically and functionally remain to be fully characterized. We recently showed that activated human Tregs express mRNA for a transmembrane protein called glycoprotein A repetitions predominant (GARP, or LRRC32). Here, using a GARP-specific mAb, we demonstrate that expression of GARP on activated Tregs correlates with their suppressive capacity.

The biology of FoxP3: a key player in immune suppression during infections, autoimmune diseases and cancer.

The Transcription factor FoxP3 belongs to the forkhead/winged-helix family of transcriptional regulators and shares general structural features with other FoxP family members. FoxP3 functions as a master of transcription for the development of regulatory T-cells (Treg cells) both in humans and in mice. Natural genetic mutations ofFoxP3 that disrupt its function in humans result in an autoimmune syndrome called Immune Polyendocrinopathy, Enteropathy, X-linked (IPEX) and in mice, its deletion causes the Scurfy phenotype, with similar pathology.