John D. and
Catherine T. MacArthur
Research Network on Socioeconomic Status and Health
Antibody Response to an Antigenic Challenge Summary prepared by Sheldon Cohen in
collaboration with the Allostatic Load Working Group. Last revised December, 1997. Cohen
and collagues have written an expanded and more detailed treatment of this topic: Cohen,
S., Miller, G. E., & Rabin, B. S. (2001). Psychological stress and antibody response
to immunization: A critical review of the human literature. Psychosomatic Medicine, 63,
7-18. The immune system responds to foreign invaders (antigens) by producing antibodies. Antibodies are protein molecules that attach themselves to invading microorganisms and mark them for destruction or prevent them from infecting cells. Antibodies are antigen specific. That is antibodies produced in response to antigen exposure are specific to that antigen. In an in vivo test assessing the competence of the humoral arm of the immune system, individuals are inoculated with an antigen, and the amount of antibody (Ab) produced in response to that specific antigen is quantified. Depending on the specific type of Ab, it can be quantified from either blood (IgG) or mucosal secretions such as saliva and nasal discharge (IgA). The more Ab produced in response to an antigen, the more "competent" the humoral system is assumed to be. It is important to distinguish between primary and secondary response to an antigen challenge. Primary response refers to the first time a persons is exposed to the antigen. Secondary response refers to subsequent exposure. Following a primary antigenic challenge there is an initial lag phase when no antibody can be detected. This is followed by phases in which the antibody titre rises logarithmically to a plateau and finally declines again as the antibodies are naturally catabolized or bind to the antigen and are cleared from circulation. The secondary response has a shorter lag phase and an extended plateau and decline. The plateau in secondary response is typically 10X greater than in primary response. Measurement Physiological Mechanisms When antigen encounters the immune system it is processed by antigen-presenting cells which retain fragments of the antigen on their surfaces. T-helper cells recognize the antigen via their surface receptors and provide help to B cells which also recognize antigen by their surface receptors. The B cells are stimulated to proliferate and divide into antibody forming cells which secrete antibody. There are a small number of antigens (T-independent antigens) that can stimulate B cells to produce Ab without T-cell help. Relevant Research There are no studies that related SES to antibody response, but a number have examined associations of antibody response (in humans) with psychological stress. All have used Hepatitis B vaccinations. Unfortunately, these data do not provide a clear picture of the role of stress in antibody response. Most of the studies have addressed response to Hepatitis B vaccinations. Glaser et al (1992) failed to find a prospective relation between negative affect and seroconversion (initial production of Hepatitis B antibodies) in response a primary challenge (first injection). They did, however, find that those who did not seroconvert were more stress reactive (reported more stress in response to a subsequent exam period) than those who did seroconvert. The other studies have all examined secondary response. Jabaaij et al (1993) found that greater perceived stress assessed after the second Hepatitis B vaccination was associated with less antibody production (among those who had already seroconverted) in response to the third injection. It is unclear, however, whether these differences in antibody level are great enough to influence the degree of protection against infection provided by the vaccination. In contrast, Petry et al (1991) found that the greater the perceived stress, irascibility, depression, and anxiety, the greater the peak antibody response. Finally, in a recently completed dissertation, Anna Marsland found that trait negative affect (also called neuroticism or emotional instability) is associated with poorer antibody response to the second vaccination. However, perceived stress (assumed to assess a state response) was not associated with response. In a single study of antibody response to influenza vaccinations, Kiecolt-Glaser et al. (1996) found that elderly caregivers for spouses with a progressive dementia (hence under chronic stress) had impaired primary response to an influenza virus vaccination when compared to matched (noncaregiver) controls. Glaser, R., Kiecolt-Glaser, J. K., Bonneau, R. H., Malarkey, W., Kennedy, S., & Hughes, J. (1992). Stress-induced modulation of the immune response to recombinant hepatitis B vacine. Psychosomatic Medicine, 54, 22-29. Kiecolt-Glaser, J.K., Glaser, R., Gravenstein, S., Malarkey, W.B., & Sheridan, J. (1996). Chronic stress alters the immune response to influenza virus vaccine in older adults. Proceedings of the National Academy of Sciences of the United States of America, 93, 3043-3047. Jabaaij. L., Grosheide, P.M., Heijtink, R.A., Duivenvoorden, H.J., Ballieux, R.E., & Vingerhoets, A.J.J.M. (1993). Influence of perceived psychological stress and distress on antibody response to low dose rDNA hepatitis B vaccine. Journal of Psychosomatic Research, 37, 361-369. Petry, L.J., Weems, L.B., & Livingston, J.N. (1991). Relationship of stress, distress, and the immunologic response to a recombinant hepatitis B vaccine. The Journal of Family Practice, 32, 481-486. |
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Contact: Judith Stewart
Revised 20 Dec 1999