Assessment Of Humoral Immune Responses Research Articles

In vitro assessment of humoral immunity following exposure to heavy metals.

The immune system of animals and man is extremely complex. This report will discuss the effect metals has on one segment of the immune system; that is, humoral immunity. Humoral immunity is essentially the production of antibody in response to an antigen. The B-lymphocyte is the primary cell responsible for producing antibody. However, this cell is regulated by T-lymphocytes and macrophages. Many methods are available to assess humoral immune responses. A multitude of immunoassays have been developed for enumeration of serum antibody. Some of these are immunodiffusion, complement fixation, serum neutralization, hemagglutination, radioimmunoassay and enzyme-linked immunosorbent assay (ELISA). Detection of antibody-forming cells distinguishes between effect on antibody production compared to degradation of preformed antibody. Other available methods are measurement of surface receptor (Fc and complement) activity on B-cells. Mitogens (T-independent) have also been regarded as a measurement for humoral immunity. In our laboratory, we have developed an ELISA technique that is appropriate for general assessment of humoral immune responses resulting from chemical exposure. This technique is highly sensitive and can be mechanized. The assay can easily be incorporated into the drug and chemical efficacy testing programs of industry.

Assessment of humoral immune responses to tumor-associated antigens

Assessment of humoral immune responses to tumor-associated antigens

Immune Response to Mycobacterium leprae: Further Studies on the Assessment of Humoral Immune Response in Mice

Immuncyte proliferation in the spleens of mice given both a primary and a second infection sixty days later, was detected soon after the second challenge was administered. Plaque-forming cell assay for both the direct and developed plaques indicated that all cells producing antibody of both immunoglobulin classes were present in the animals when they were administered the second challenge. Hemagglutinating antibody determinations indicated that IgG antibodies are recognizable at a time when the bacilli reach a stage of maximum multiplication in the mouse host. The IgM antibodies, however, become detectable within a short time after infection in animals given either a single infection or a dual infection, one fifteen days later and the other sixty days after the first infection. It is proposed that the low level of circulating antibodies and antibody-producing cells despite continuous, as well as enhanced, antigenic challenge could be due to the fact that in the mouse footpad M. leprae may be intrinsically less antigenic than organisms that cause systemic infection. Quantitative immunoglobulin assays tended to confirm the observations on the HA studies. Present studies have once again confirmed our previous observations viz that the number of plaques in the spleens of mice infected with M. leprae increases on secondary stimulation, whether it is administered within a very short time after the primary infection or given later in the course of infection. They have also indicated that an IgG response will occur in the infected animals at a time when the bacillary multiplication enters the logarithmic phase of growth of M. leprae, They have, however, not permitted the placement of the mouse model in the overall spectrum of human leprosy.