The female humoral and cell mediated immune system response is on average more active than males and in theory may account for the increased longevity of women (Grossman 1989). In general, women are far better than men in fighting off bacterial and viral infection (Janeway 1993), but a more sensitive immune system will be more likely to develop autoimmune activity. Typically, autoimmune disease is far more common in females than males (Ollier 1992). Hormones including gonadal steroids, adrenal glucocorticoids, thymic hormones and prolactin are known to influence lymphocyte activity – but the most potent hormone affecting the immune system directly and indirectly is estrogen (Grossman 1989, Schuurs 1990).
Allergies are classed as hypersensitivity reactions – an inappropriate over-reaction to foreign antigens whereas autoimmune diseases are an inappropriate over-reaction to self antigens. Extensive studies into allergy susceptibility show that for women the first symptoms most often occur between the ages of 10 and 29 (Wormald 1977) and laboratory/in vitro studies have shown that estrogen can directly stimulate lymphocytes and cytokine chemical signal production (Stimson 1988, Schuurs 1990, Fox 1991). Consequently, the hormonal changes at and after puberty are believed to increase an individual’s immune system sensitivity and lead to increased potential for autoimmune disease development (Grossman 1989, Schuurs 1990). It is possible similar mechanisms are at work in AA.
Women with AA can sometimes go into spontaneous, temporary remission when pregnant (Sulen 1956 in Rook 1991, Muller 1963). Equally, women have reported the first onset of AA during pregnancy (Muller 1963). Presumably induction or remission is due to the associated fluctuations in hormone levels.
