Sex differences and estrogen modulation of the cellular immune response after injury

Abstract

Cell-mediated immunity is extremely important for resolution of infection and for proper healing from injury. However, the cellular immune response is dysregulated following injuries such as burn and hemorrhage. Sex hormones are known to regulate immunity, and a well-documented dichotomy exists in the immune response to injury between the sexes. This disparity is caused by differences in immune cell activation, infiltration, and cytokine production during and after injury. Estrogen and testosterone can positively or negatively regulate the cellular immune response either by aiding in resolution or by compounding the morbidity and mortality. It is apparent that the hormonal dysregulation is dependent not only on the type of injury sustained but also the amount of circulating hormones. Therefore, it may be possible to design sex-specific therapies to improve immunological function and patient outcome.

Role of Estrogen Supplementation in Boosting the Immune Response and Stress Resistance as Seen in the White Pulp of the Senile Female Albino Rat Spleen

“…Thus, Estrogen administered prior to stress exposure resulted in T cell preservation. The present data is in accordance with previous reports (Bird et al, 2008;Sármay et al, 2010). Immune staining with anti-CD20 antibody for groups C and D revealed weak reaction in the two groups with more negative reaction in group C. Stress per se results in humoral immune response which implies the activation and differentiation of B lymphocytes into the antibody producing plasma cell with resultant decrease in the number of resting B cells (Verthelyi & Ahmed, 1998;Bynoe et al, 2000;Guéguinou et al, 2011).…”

“…This observation was further documented by immune staining for CD3 and CD20 that revealed marked increase in the number of positively stained cells. The present findings are in accordance with previous reports on the immune stimulatory effect of estrogen administration (Bird et al, 2008;Cunningham & Gilkeson, 2011). Cesta (2006) commented that aging could decrease lymphocytes numbers by 80%.…”

A high corticosterone/DHEA-s ratio in young rats infected with Trypanosoma cruzi is associated with increased susceptibility

“…In line with other reports, this aromatisation could promote increased oestrogen levels (Spratt et al 2006), which would further restrict T. cruzi growth (do Prado et al 1998). The present data ( Figs 2B, 4A, 5B) concerning high levels of oestrogen accompanied by a low T/E 2 ratio in adult rats fit well with an endocrine adaptive condition that favours an effective cellular and humoral immune response (Wilder & Elenkov 1999, Elenkov et al 2000, Bird et al 2008). …”

Redox Regulation of T-Cell Function: From Molecular Mechanisms to Significance in Human Health and Disease

“…Comparison of AICD in MART-1 [27][28][29][30][31][32][33][34][35] and MP [58][59][60][61][62][63][64][65][66] epitope-specific primary (1°) and secondary (2°) expanded CTLs. CTL populations were stimulated with control and cognate epitope, and AICD was measured using annexin V staining (histogram).…”