Here's a study that points to males having weaker immune systems than females.
Hormonal Flux During Physiological Development & Immune Strength
[Autism may be an immune disorder in response to environmental
assaults. Source: American Physiological Society.]
http://www.faseb.org/aps/
http://www.sciencedaily.com/releases/2001/10/011022030942.htm
It is generally recognized among immunologists that males of all
species have lower immunity than females. Men are more susceptible to a
variety of infections, such as dysentery, gonorrhea, and malaria; and to
certain cancers. Females are at greater risk of illnesses caused by an
overactive immune system, such as systemic lupus erythematosus, diabetes
ulcerative colitis, and arthritis. Why men and women respond differently to
infections caused by viruses or other parasites remains a mystery.
How the immune system adopts certain strategies towards particular
illnesses has not been determined. Examining gender characteristics,
hormones and genes, and how they interact with immunology could provide
answers to these questions. This was the goal of a team of Johns Hopkins
researchers as they set out to determine how differences in sex are
expressed in rats' response to hantaviruses (sex differences in hantaviruses
represent an ecologically and clinically relevant model for studies of
sex-based differences in infection).
Researchers Sabra L. Klein, Ph.D., A.L. Scott, and G.E. Glass, Ph.D.,
all from the Department of Molecular Microbiology and Immunology, The Johns
Hopkins University Bloomberg School of Public Health, Baltimore, Md., have
conducted a study on "Sex Differences in Hantavirus Infection: Interactions
Among Hormones, Genes, and Immunity."
Their findings are to be presented at the conference, Genomes and
Hormones: An Integrative Approach to Gender Differences in Physiology, being
sponsored by the American Physiological Society (APS) October 17-20, 2001,
at the Westin Convention Center, Pittsburgh, Pa.
Methodology and Results
These researchers first set out to determine if manipulating sex
steroids in adult rodents would impact the response to inoculation with the
Seoul virus (a Hantavirus that naturally occurs in Norway rats). The
researchers found that in the male rats, the production of antibodies
increased, enhanced Th1 responses (inflammatory responses) against infection
occurred, and shed or released the virus into the environment for a longer
time period than comparable females in the study. Accordingly, hormone
manipulation in female and male adult rodents had no effect on their normal
response to virus infection.
In all animals (including humans), sex steroid hormones affect
gender-specific development at two distinct times. During perinatal (i.e.,
during prenatal and early postnatal) development, sex steroids cause
permanent, hard-wired differences in the organization of central and
peripheral physiology (i.e., organizational effects). After puberty,
exposure to sex steroids serves to transiently activate pre?existing
hormonal circuits (i.e., activational effects). In mammals, masculine
development is induced by early exposure to testosterone, whereas feminine
development occurs in the absence of testosterone. Because manipulation of
hormones in adult animals had no effect on responses to viral infection,
these researchers hypothesized that hormones may hard-wire gender-specific
immune responses earlier during development.
Therefore, the next step in the study was to determine if neonatal
manipulation of sex hormones organized adult responses to the hantavirus
administered to rats. After two to four days of age, male rats were
castrated and females were injected with testosterone. All animals were
inoculated with the Seoul virus as adults; antibody responses and viral
prevalence were assessed in both sexes.
Castrated males displayed female-type responses, i.e. lower
concentrations of anti-virus responses with less virus shed than in the
control male population. On the other hand, injecting testosterone into
female neonatal mice had no impact on that group's response to infection.
Conclusions
Altering the immune response to infection occurs at a neonatal stage,
as evidenced by the lowering levels of testosterone in male mice. However,
manipulating testosterone levels in female mice had no impact on the immune
system. These results suggest that the preponderance of gender-related
immunological diseases must be related to mechanisms other than sex steroids
alone, possibly genetic differences between the sexes.
