Tumors humoral immune response

Brichory, F., et al., "Proteomics-Based Identification of Protein Gene Product 9.5 as a Tumor Antigen that Induces a Humoral Immune Response in Lung Cancer," Cancer Res., 61, 7908-7912 (2001). 

Urso, P., and Gengozian, N. Subnormal expression of cell-mediated and humoral immune responses in progeny disposed toward a high incidence of tumors after in utero exposure to benzo[a]pyrene, J. Tox. Environ. Health, 14, 569, 1984. 

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. 

Brichory F, Beer D, Le Naour F, Giordano T, Hanash S. (2001) Proteomics-based identification of protein gene product 9.5 as a tumor antigen that induces a humoral immune response in lung cancer. Cancer Res 61, 7908-12. 

These mature, but naive T cells exit peripheral blood and seed lymphoid organs in T-cell specific zones to be acquired by adaptive immune responses for elimination of infected or tumor cells, support for humoral immune responses, formation of immunologic memory, prevention of excessive tissue damage, and facilitation of tissue regeneration (see Chapter 12). 

Induction of humoral, cellular, and mucosal immunity. For prophylactic vaccination, all three types of immune response should be addressed. Vaccination against diseases caused by viruses or other intracellular pathogens essentially requires a strong induction of cellular immunity, whereas bacteria-borne diseases need a strong induction of the humoral immune response. For therapeutic vaccination, and especially for tumor treatment, a strong induction of cellular immunity is desirable [6]. 

Heavy Metals. Some heavy metals such as gold and platinum are used pharmacologically as immunomodulators to treat rheumatoid arthritis and as antineoplastic drugs, respectively. Most heavy metals inhibit mitogenicity, antibody responses, and host resistance to bacterial or viral challenge, and tumor growth. Platinum has been shown to suppress humoral immunity, lymphocyte proliferation, and macrophage function (Lawrence, 1985). Clinically, mild to moderate myelosuppression may also be evident with transient leukopenia and thrombocytopenia. 

The mode of association of peptides to liposome carriers might also be critical to induce a preferential immune response either humoral or cell mediated. For example, using a human mucin MUCl 20-mer peptide, it was found that only the physical association of the peptide to liposomes (either encapsulated or surface exposed after anchoring) was necessary to observe a cell-mediated response (34). In line with this observation, it was recently shown that a soluble peptide, representing a Melan-A/MART-1 tumor-associated antigen, when encapsulated into sterically stabilized liposomes, was able to stimulate a CTL response and this construct represented a suitable formulation for a specific tumor immunotherapy (69). In contrast, and in agreement with other studies (16), only the liposome surface exposed... 

In addition to monoclonal antibody or chemotherapy, immunotherapy has been developed to target tumor antigen for the treatment of FL. The unique sequence of the protein, so-called idiotype (Id) protein, can be a target of immunotherapy. Because Id protein can induce humoral and cellular immune responses against idiotype protein, vaccination with Id protein can decrease the risk of progression. However, the mechanism of anti-Id response has been unclear. 

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