Gender differences in host defense mechanisms

Abstract

Extensive studies in both humans and animals have shown that females express enhanced levels of immunoreactivity compared to males. Whereas this provides females with increased resistance to many types of infection, it also makes them more susceptible to autoimmune diseases. This review will focus on gender-related differences in non-specific host defense mechanisms with a particular emphasis on monocyte/macrophage function and a primary product of monocytes: interleukin-1 (IL-1). ∗ ∗ Interleukin-1 has two agonist forms (α and β) that bind to the same receptors and have virtually identical biological activities. Many of the reports cited in this review used bioassays that do not distinguish between the two forms, therefore the generic term IL-1 is used in most cases. Two forms of tumor necrosis factor (TNF) also exist. In this review, TNF always refers to the α form (also known as cachectin). Other abbreviations used in this review are: CFS — chronic fatigue syndrome; Ig — immunoglobulin; SLE — systemic lupus erythematosus; IDDM — insulin dependent diabetes mellitus; MØ — macrophage(s); Th1, Th2 — T helper 1, 2; IFN γ — interferon γ; LH — luteinizing hormone; FSH — follicle stimulating hormone; PG — prostaglandin; CRF — corticotrophin-releasing factor; ACTH — adrenocorticotrophic hormone; HPA — hypothalamic-pituitary-adrenal; GnRH — gonadotropin-releasing hormone; PRL — prolactin; E — estrogen; P — progesterone; DES — diethylstilbestrol. Immunomodulatory cytokines such as IL-1 are influenced by gender-sensitive hormones, and reciprocally, these cytokines influence gender-specific hormones and tissues. Patients with chronic fatigue syndrome (CFS) are predominantly women, therefore it may be useful to look toward gender-specific differences in immune function to find a key for this poorly understood syndrome.