Clinical & Medical Biochemistry

Immunosuppressive Therapeutic Approaches for Managing Inflammation and Improving Outcomes in Villitis of Unknown Etiology (VUE)

Geoff Dillon^* Department of Immunology, University of Melbourne, Parkville, Australia
^*Correspondence: Geoff Dillon, Department of Immunology, University of Melbourne, Parkville, Australia, Email:

Received: 03-Jul-2023, Manuscript No. CMBO-23-22625; Editor assigned: 06-Jul-2023, Pre QC No. CMBO-23-22625 (PQ); Reviewed: 20-Jul-2023, QC No. CMBO-23-22625; Revised: 27-Jul-2023, Manuscript No. CMBO-23-22625 (R); Published: 03-Aug-2023, DOI: 10.35841/2471-2663.23.9.180

Description

The placenta, a multifunctional organ essential for maternal-fetal exchange and fetal development, is susceptible to various immune-mediated disorders that can impact pregnancy outcomes. One such enigmatic condition is Villitis of Unknown Etiology (VUE), characterized by the infiltration of immune cells into the placental villous tissue. VUE is a rare and perplexing placental condition characterized by the presence of chronic inflammatory infiltrates, predominantly composed of T lymphocytes, within the villous tissue.

Despite its classification as "villitis of unknown etiology," various factors such as infections, immunological factors, and genetic predisposition have been suggested to contribute to its pathogenesis. Clinically, VUE is associated with adverse pregnancy outcomes, including Intrauterine Growth Restriction (IUGR), preterm birth, and fetal distress. Histopathologically, VUE is characterized by the presence of lymphocytic infiltrates within the chorionic villi, often accompanied by varying degrees of intervillositis and fibrinoid necrosis.

Transplant immunology provides a well-established framework for understanding immune responses against allogeneic grafts and can offer valuable insights into immune-mediated processes that may contribute to VUE. In organ transplantation, the recipient's immune system recognizes donor antigens as foreign, triggering a series of immune responses that can lead to graft acceptance, rejection, or tolerance.

Drawing parallels between transplant rejection and the immune response in VUE can provide new perspectives on the pathogenesis of VUE. In VUE, the placental villi encounter immune cells that respond to unknown antigens, analogous to allorecognition in transplantation. Innate immune cells, including macrophages and natural killer cells, infiltrate the placental tissue, triggering an inflammatory cascade. Subsequent adaptive immune responses, involving T and B lymphocytes, contribute to the chronic inflammatory milieu observed in VUE. This interplay between innate and adaptive immunity mirrors the complexity of the immune response seen in organ transplantation.

Human Leukocyte Antigen (HLA) molecules play a pivotal role in transplant rejection by mediating allorecognition and immune responses against allografts. In VUE, alterations in HLA expression within the placenta may trigger immune reactions. Maternal T cells recognizing paternal HLA antigens could potentially contribute to the immune response and placental inflammation observed in VUE, akin to graft-versus-host reactions seen in stem cell transplantation. Cytokines play a central role in orchestrating immune responses and inflammation. In both transplantation and VUE, a delicate balance of pro-inflammatory and anti-inflammatory cytokines influences the immune milieu. Pro-inflammatory cytokines, such as Tumor Necrosis Factor-Alpha (TNF-α) and Interleukin-6 (IL-6), contribute to tissue damage and inflammation. Regulatory cytokines, such as Transforming Growth Factor-Beta (TGF-β), attempt to restore immune homeostasis.

Dysregulation of these cytokines can lead to chronic inflammation, a hallmark of both VUE and transplant rejection. T regulatory (Treg) cells are critical in maintaining immune tolerance and preventing excessive immune responses. In transplantation, Treg cells play a role in immune regulation and can influence graft acceptance or rejection. Similarly, Treg cells may play a role in placental immune tolerance, and alterations in Treg cell function could contribute to the immune dysregulation and inflammation observed in VUE. Understanding the immunopathological parallels between VUE and transplant rejection holds significant implications for diagnosis and treatment. Biomarkers used in transplant rejection, such as soluble HLA antigens or cytokine profiles, could be investigated for their relevance in diagnosing and monitoring VUE.

Conclusion

Strategies employed in transplantation to modulate immune responses, such as immunosuppressive therapies, might offer avenues for managing inflammation and improving outcomes in VUE cases. As our understanding of immune-mediated processes in pregnancy advances, innovative diagnostic tools and therapeutic approaches may emerge, ultimately leading to improved outcomes for mothers and infants affected by VUE. The application of transplant immunology concepts to VUE, illustrates the potential for interdisciplinary collaboration to solve the complexities of placental disorder.