Sexual dimorphism of humoral immunity with human vaccines.
ABSTRACT It has been contended that limited data exist on sex-difference in immune response with vaccines in humans. However, a comprehensive search of the literature retrieved 97 studies with 14 vaccines influenza (7 studies), hepatitis A (15 studies), hepatitis B (50 studies), pnuemococcal polysaccaride (4 studies), diphtheria (4 studies), rubella (3 studies), measles (2 studies), yellow fever (3 studies), meningococcal A (1 study), meningococcal C (1 study), tetanus (1 study), brucella (1 study), Venezuelan equine encephalitis (1 study) and rabies (4 studies), with sex-difference in humoral (antibody) response. These differences are associated with sex-difference in the clinical efficacy of influenza, hepatitis A, hepatitis B, pneumococcal polysaccharide and diphtheria vaccines and significant adverse reactions with rubella, measles and yellow fever vaccines. The genesis of these differences is uncertain but not entirely related to gonadal hormones (differences are seen in pre-pubertal and post-menopausal subjects not on hormone replacement therapy) or female sex (males had greater serological response for pneumococcal, diphtheria, yellow fever, Venezuelan equine encephalitis and in some studies with rabies vaccine. As sex-difference in humoral immune response was seen with most vaccines which cover the spectrum of mechanisms by which infectious agents cause disease (mucosal replication, viral viraemia, bacterial bacteraemia, toxin production and neuronal invasion), it is mandatory that vaccine trialists recruit a representative sample of females and males to be able to assess sex-differences which may have clinical implications.
SourceAvailable from: Eric Christopher Shattuck[Show abstract] [Hide abstract]
ABSTRACT: Sickness behavior, a coordinated set of behavioral changes in response to infection, lies at the intersection of immunology, endocrinology, and evolutionary biology. Sickness behavior is elicited by pro-inflammatory cytokines, is thought to be an adaptive means of redirecting energy away from disadvantageous behaviors and toward mounting an effective immune response, and may be modulated by hormones, including testosterone and oxytocin. Research on sickness behavior in humans has lagged behind non-human animal research due to methodological complexities. Here we review what is known about sickness behavior in humans, the effects of various hormones on sickness behavior, the possible role of cytokine gene variation in influencing sickness behavior responses, and the ways in which culture and gender norms could similarly influence these behavioral changes. We also propose methodologies for advancing further studies of sickness behavior in humans.American Journal of Physical Anthropology 01/2015; DOI:10.1002/ajpa.22698 · 2.51 Impact Factor
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ABSTRACT: Many theories of autoimmune disease have been proposed since the discovery that the immune system can attack the body. These theories include the hidden or cryptic antigen theory, modified antigen theory, T cell bypass, T cell-B cell mismatch, epitope spread or drift, the bystander effect, molecular mimicry, anti-idiotype theory, antigenic complementarity, and dual-affinity T cell receptors. We critically review these theories and relevant mathematical models as they apply to autoimmune myocarditis. All theories share the common assumption that autoimmune diseases are triggered by environmental factors such as infections or chemical exposure. Most, but not all, theories and mathematical models are unifactorial assuming single-agent causation of disease. Experimental and clinical evidence and mathematical models exist to support some aspects of most theories, but evidence/models that support one theory almost invariably supports other theories as well. More importantly, every theory (and every model) lacks the ability to account for some key autoimmune disease phenomena such as the fundamental roles of innate immunity, sex differences in disease susceptibility, the necessity for adjuvants in experimental animal models, and the often paradoxical effect of exposure timing and dose on disease induction. We argue that a more comprehensive and integrated theory of autoimmunity associated with new mathematical models is needed and suggest specific experimental and clinical tests for each major theory that might help to clarify how they relate to clinical disease and reveal how theories are related. Copyright © 2014. Published by Elsevier Ltd.Journal of Theoretical Biology 12/2014; DOI:10.1016/j.jtbi.2014.11.022 · 2.30 Impact Factor
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ABSTRACT: The immune systems of men and women differ in significant ways, especially after puberty. In particular, females are generally more prone to autoimmunity, but experience lower rates of infections and chronic inflammatory disease. Sex hormones, genes encoded on the sex chromosomes, and gender-specific behaviors likely contribute to these differences. The aging process is associated with changes in the composition and function of the immune system and these changes may occur at an accelerated rate in men as compared to women. Moreover, after the age of menopause, the incidence of chronic inflammatory disease in women approaches or exceeds that observed in males. At the same time, the incidence of autoimmunity in post-menopausal women is decreased or equivalent to the rates observed in similarly-aged men. Additional studies addressing the influence of sex on the pathogenesis of chronic and autoimmune diseases in the aged are warranted. Copyright © 2015 Elsevier Inc. All rights reserved.Cellular Immunology 02/2015; 294(2). DOI:10.1016/j.cellimm.2015.02.002 · 1.87 Impact Factor