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ICAM-1 expression on immune cells in chronic villitis
E S A Egal1, F V Mariano1, M H Blotta2
1Department of Pathology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), São Paulo, Brazil.
Insights
Immune cell Intercellular Adhesion Molecule-1 (ICAM-1) expression in chronic villitis (CV) is high in perivillous regions and low within villi. Trophoblast rupture amplifies inflammation, with ICAM-1 on immune cells near rupture sites.
Area of Science:
- Immunology
- Reproductive Biology
- Pathology
Background:
- Intercellular Adhesion Molecule-1 (ICAM-1) on syncytiotrophoblast (ST) is implicated in maternal cell migration into inflamed villi.
- ICAM-1's role on immune cells within chronic villitis (CV) villi remains uncharacterized.
- ICAM-1 mediates cell adhesion, T cell defense, and inflammatory responses.
Purpose of the Study:
- To investigate ICAM-1 expression on immune cells in chronic villitis (CV).
- To correlate ICAM-1 expression with immune cell location and trophoblastic integrity in CV.
Main Methods:
- Analysis of 21 CV placentas and 3 controls for ICAM-1, CD45, CD3, and CD68.
- Immune cells were categorized as within inflamed villi or in perivillous aggregates.
- Immunohistochemistry was used to assess protein expression and cell location.
Main Results:
- High CD45, CD3, and CD68 expression was observed within villi and in perivillous aggregates near trophoblastic loss.
- ICAM-1 was frequently expressed on ST in inflamed villi.
- Immune cells near trophoblastic rupture sites showed strong ICAM-1 expression, unlike those within villi.
Conclusions:
- Immune cell ICAM-1 expression in CV is location-dependent: high in perivillous regions, low within villi.
- Strong ICAM-1 expression on immune cells at trophoblastic rupture sites suggests amplified inflammation.
- Trophoblast loss may drive increased inflammatory response via ICAM-1 signaling.
Introduction:
ICAM-1 expression on the villous syncytiotrophoblast (ST) is believed to participate in migration of maternal cells into the inflamed villi regardless of villitis etiology. However, its expression on immune cells in chronic villitis (CV) has yet to be analyzed. ICAM-1 induces cell-cell adhesion allowing intercellular communication, T cell-mediated defense mechanism, and inflammatory response.
Material And Methods:
21 cases of CV (all without an identifiable etiologic agent) and 3 control placentas were analyzed using ICAM-1, and for immune cells CD45, CD3 and CD68. These cells were subdivided according to their location in inflamed villi: a) within the inflamed villi and b) outside forming perivillous aggregates.
Results:
Large amounts of CD45, CD3 and CD68 were found within the inflamed villi and forming perivillous aggregates attached to areas of trophoblastic loss. Inflamed villi usually showed ICAM-1+ ST. The majority of immune cells surrounding areas of trophoblastic rupture presented marked expression of ICAM-1. In contrast, a small number of immune cells within the inflamed villi exhibited ICAM-1 expression. Only some (<5%) inflamed villi without trophoblastic rupture and with ICAM-1+ ST presented adherence of immune cells.
Discussion:
In inflamed villi of chronic villitis, the level of ICAM-1 expression on immune cells depends on their location: high in number of cells in the perivillous region and low within the villi. The strongest expression of ICAM-1 on immune cells attached to areas of trophoblastic rupture suggests that the loss of trophoblast can lead to an amplification of the inflammatory response.
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