Helper cells

Gradual diminution of 004 T-lymphocytes from the peripheral blood is the most consistent feature observed in HIV infection. Because the majority of 004 cells are T-helper lymphocytes, removal leads to deficiency of cellular immunity, which depends on T-helper cells to initiate cytotoxic T-ceU killing of vims-infected cells of cancer. The loss of immune surveillance leads to the appearance of viraHy induced tumors from unopposed clonal expansion of viraHy transformed cells. Furthermore, depletion of cellular immunity leads to exaggerated viral, fungal, and proto2oal infections. 

In addition to antibodies, the immune system also consists of bone-marrow derived lymphocytes, or B cells, and T cells that come from the thymus gland, both of which (indirectly) produce antibodies. These cells, in turn, may be helped by helper cells (= H) and suppressed by suppressor cells (= S). Helper cells may be alarmed as to the presence of antigens by macrophages (= M) that eat the antigens and leave parts of their meal on their cell surface. 

We can interpret these equations in the following way. The first line assures us that antibodies will be present only when B cells, helper cells and antigens are all present. The second line states that B cells will grow if antigens and/or B cells are present and if helped by helper cells. The third line indicates that helper cells arise either if other helper cells ai e present or, if no suppressor cells are present, if there are any antigens. The fourth line yields suppressor cells if suppressor cells are already present and/or there are any helper cells. The last line implies that the antigen remains if there are no antibodies or vani.shes if antibodies are present. Since concentrations cannot exceed 1, it is understood that, in the above equations, 1 + 1 = 1. 

Now suppose the body s immune system malfunctions and begins attacking the body itself. A typical scenario might involve killer cells K attacking helper and/or suppressor cells. Chowdbury and Stauffer [chowdQO] developed a simple five-cell model using two types of helper cells Hi and H2). two type of suppressors Si and S2) and one killer cell (K) ... 

In patients infected with HIV (human immunodeficiency virus), the helper cell population is weakened to the point where the immune system is no longer able to function properly. The body thus becomes susceptible to otherwise nonlethal diseases such as pneumonia. 

The first equation states that cytotoxic cells grow only if helper cells, macrophages and the virus are all present. The second equation implies that, when the virus is not present, helper cells grow if macrophages and/or helper cells are present. The third equation implies that macrophages grow both when the virus is present and there is already a concentration of macrophages. The last equation describes the... 

AIDS (acquired immunodeficiency syndrome) is the final stage of disease caused by infection with HIV. In this stage, the vims infection has severely affected the immune system, causing a depletion of CD4+ T-helper cells. AIDS is characterized by the manifestation of typical diseases caused by opportunistic infections (Pneumocystis carinii pneumonia, CMV retinitis, candidiasis of the esophagus, cerebral toxoplasmosis), neurological manifestations, cachexia, or certain tumors (Kaposi sarcoma of the skin, B-cell lymphoma). 

ADM may evolve over several years, the extent of fiber atrophy provides an important indication of the chronicity of muscle degeneration. Acute muscle necrosis and phagocytosis give some indication as to how active the disease is at the time of biopsy. In most biopsies from ADM patients, the inflammatory cell foci are perivascular and perimysial rather than endomysial and are dominated by B-lymphocytes. The ratio of T4 lymphocytes (helper cells) to T8 lymphocytes (cytotoxic) generally indicates a predominance of the former. As in JDM, this is consistent with humoral mechanisms of cell damage, and vascular involvement is also apparent in the form of capillary endothelial cell abnormalities (tubular arrays) and duplication of basal lamina. Loss of myofibrillar ATPase from the central portions of fibers is a common prelude to muscle necrosis. 

An increased ratio of T suppressor cells to T helper cells was seen in mice given 2.5 and 5.0 mg/kg/day of methyl parathion for 15 days the spleen to body weight ratio was increased at 5 mg/kg/day (Tian et al. 1997). No other immunological or lymphoreticular end points were measured. 

Briere F, de Waal Malefyt R, Liu YJ Reciprocal control of T-helper cell and dendritic cell differentiation. Science 1999 283 1183-1186. 

Cause WC. Urban JF. Linsley P. Lu P Role of B7 signaling in the differentiation of naive CD4+ T cells 122 to effector interIeukin-4-producing T-helper cells. Immunol Res 1995 14 176-188. 

Roy S, Cain KJ, Chapin RB, Charboneau RG, Barke RA (1998) Morphine modulates NF kappa B activation in macrophages. Biochem Biophys Res Commun 245 392-396 Roy S, Wang J, Gupta S, Charboneau R, Loh HH, Barke RA (2004) Chronic morphine treatment differentiates T helper cells to Th2 effector cells by modulating transcription factors GATA 3 and T-bet. J Neuroimmunol 147 78-81... 

Astaxanthin has a significant enhancing action on the production of immunoglobulins A, M, and G and on T helper cell antibody production, even when subop-timal amounts of antigen are present. 

Yoneyama H, Narumi S, Zhang Y, et al. Pivotal role of dendritic cell-derived CXCL10 in the retention of T helper cell 1 lymphocytes in secondary lymph nodes. J Exp Med 2002 195(10) 1257-1266. 

Hardtke S, Ohl L, Forster R. Balanced expression of CXCR5 and CCR7 on follicular T helper cells determines their transient positioning to lymph node follicles and is essential for efficient B-cell help. Blood 2005 106 1924-1931. 

Bonecchi R, Bianchi G, Bordignon PP, et al. Differential expression of chemokine receptors and chemotactic responsiveness of type 1 T helper cells (This) and Th2s. J Exp Med 1998 187 129-134. 

Sato N, Ahuja SK, Quinones M, et al. CC chemokine receptor (CCR)2 is required for langerhans cell migration and localization of T helper cell type 1 (Thl)-inducing dendritic cells. Absence of CCR2 shifts the Leishmania major-resistant phenotype to a susceptible state dominated by Th2 cytokines, b cell outgrowth, and sustained neutrophilic inflammation. J Exp Med 2000 192(2) 205-218. 

The interleukin-2 receptor (IL-2R) is important in that the cytokine IL-2, secreted by a subset of T-helper cells, enhances the proliferation of activated T and B cells and increases the cytolytic activity of natural killer (NK) cells and the secretion of IgG. 

T Helper Cell Cytokine Responses During Intestinal Nematode Infection Induction, Regulation and Effector Function... 

Artis, D., Humphreys, N.H., Bancroft, A.J., Rothwell, N.J., Potten, C.S. and Grencis, R.K. (1999a) TNF-a is a critical component of IL-13-mediated protective T helper cell type 2 responses during helminth infection. Journal of Experimental Medicine 190, 953-962. 

Harris, N.L., Peach, R.J. and Ronchese, F. (1999) CTLA-4-Ig inhibits optimal T helper cell development but not protective immunity or memory response to Nippostrongylus brasiliensis. European Journal of Immunology 29, 311-316. 

Karpus, W.J., Lukas, N.W., Kennedy, K.J., Smith, W.S., Hurst, S.D. and Barrett, T.A. (1997) Differential C-C chemokine-induced enhancement of T helper cell cytokine production. Journal of Immunology 158, 4129-4136. 

Louahed, J., Kermouni, A., van Snick, J. and Renauld, J.C. (1995) IL-9 induces expression of granzymes and high affinity IgE receptor in murine T helper cell clones. Journal of Immunology 154, 5061-5070. 

O Garra, A. (1998) Cytokines induce the development of functionally heterogeneous T helper cell subsets. Immunity 8, 275-283. 

Subramanian, G., Kazura, J.W., Pearlman, E., Jia, X., Malhorta, I. and King, C.L. (1997) B7-2 requirement for helminth induced granuloma formation and CD4 type 2 T helper cell cytokine expression. Journal of Immunology 158, 5914-5920. 

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