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Immunology of the Acquired Immunodeficiency Syndrome

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Immunology of the Acquired Immunodeficiency Syndrome Henry Ford Hospital Medical Journal Volume 32 Number 2 Article 6 6-1984 Immunology of the Acquired Immunodeficiency Syndrome Patrick W. McLaughlin Carl B. Lauter Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation McLaughlin, Patrick W. and Lauter, Carl B. (1984) "Immunology of the Acquired Immunodeficiency Syndrome," Henry Ford Hospital Medical Journal : Vol. 32 : No. 2 , 107-115. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol32/iss2/6 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hospital Med J Vol. 32, No. 2, 1984 Immunology of the Acquired Immunodeficiency Syndrome Patrick W. McLaughlin, MD* and Carl B. Lauter, MD** The Acquired Immunodeficiency Syndrome (AIDS) first known to cause immunodeficiency. Simian AIDS, an recognized in 1981, has been extensively studied, and animal model of virus-induced immunodeficiency, is the most recent studies have demonstrated that its also discussed. Recommendations are made regarding defects extend well beyond the apparent deficient the interpretation and limitations of immune testing in cell-mediated immunity to include humoral immunity, AIDS, includinga discussion of how apparently healthy autoimmunity, and abnormal immunoregulation. The homosexuals and groups at risk develop an immu­ recent discovery ofa retrovirus, HTLV III, as a possible nologic profile which mimics that of patients with AIDS. etiologic agent is discussed in relation to other viruses J\r\ce late 1981, an unexpected outbreak of oppor­ The immune system has "surveillance" functions to tunistic infections and unusual neoplasms has been protect humans (and other vertebrates) from infections noted, described, and studied (1-4). This outbreak ap­ and cancer. Multipotential stem cells arise during em- pears to have had its onset in the United States in bryogenesis and develop further into two major popu­ 1978-1979. The affected patients lacked the usual con­ lations of lymphoid stem cells (5-8). One ofthese, pre-T genital or acquired immunosuppressive background cells, leaves the bone marrow, enters the epithelial illnesses that would be expected to predispose to such thymus, and matures there into mature T-cells under infections as Pneumocystis pneumonia and such neo­ the influence of local thymic hormones. Mature T-cells plasms as disseminated aggressive Kaposi's sarcoma. leave the thymus and populate the paracortical and The term "acquired immunodeficiency syndrome" medullary areas of lymph nodes, the central regions of (AIDS) is partially inaccurate, since it does not really the periarterial lymphoid sheaths of the spleen, and differentiate the current syndrome from many known other sites. T-cells recognize foreign antigens and self acquired immunodeficiency states such as leukemia, because of receptors on their surfaces. This system is lymphoma, systemic lupus erythematosus, and mal­ genetically controlled. A variety of T-cell surface anti­ nutrition. In addition, exogenous factors such as gens can be identified using monoclonal antibodies, and treatment with corticosteroids and other immune these antibodies can define T-cell subpopulations (5). suppressing medications can cause acquired immu­ nodeficiency. Perhaps a more descriptive (albeit, more cumbersome) term could be the "idiopathic" acquired B-cells mature in the bone marrow of mammals. The immunodeficiency syndrome. This report will attempt cell membrane ofthese cells incorporates IgD and IgM, to summarize and review the immunologic abnormali­ and these serve as recognition units for antigen(s). ties that have been described in AIDS and its apparently After specific antigenic stimulation, B-celis, usually related disorders. We will also review such immu­ under the influence of helper T-cells, undergo blastic nologic data as are available in normal healthy controls transformation, proliferate, and differentiate further. and high-risk groups, eg, homosexual men, intra­ Diversification occurs, and the five classes of immu­ venous drug users, and hemophilia patients. noglobulins are produced and secreted. The B-cells mature further into plasma cells which secrete either IgG, IgM, IgA, IgD, or IgE in varying quantities. General Overview of the Immune System The immune system is complicated, and concepts of its ongins, functions, controls, and derangements are continuously changing. Newer tools, such as hybrid- Submitted for publication: May 29, 1984 oma-produced monoclonal antibodies to cell surface Accepted for publication: July 13, 1984 markers on lymphocytes and other effector cells have •Senior Resident, Internal Medicine, William Beaumont Hospital; Currently provided more information, yet raised more questions. Fellow, Hematology-Oncology, University of Michigan Medical Center; The simplified outline of the immune system which ••Chief of Medical Services, William Beaumont Hospital, and Associate Clinical Professor of Medicine, Wayne State University School of Medicine follows will serve as a ground for the discussion that Address reprint requests to Dr. Lauter, Department of Medicine, William follows. Beaumont Hospital, 3601 W. 13 Mile Road, Royal Oak, Ml 48072, 107 McLaughlin and Lauter T-cells recognize antigen(s) and a self marker, la, coded their surface of certain class II histocompatibility mol­ by the HLA-D region in the major histocompatibility ecules that are needed for the presentation of foreign system. This encounter results in the blastic transfor­ antigens. mation and proliferation of specific T-cell clones. B-cell activation cell division requires B-cell growth However, in contrast to the change described for the factor which is produced by T-cells and interleukin-1. B-cells, several T-cell subpopulations have specific Additional lymphokines, called B-cell differentiation functions, eg, memory, suppressor activity, helper factors, are then needed to stimulate the B-cells to a activity, cytotoxicity, and lymphokine production. A state where they can produce antibodies. number of lymphokines (soluble mediators or hor­ mones released by lymphocytes that influence other In the peripheral blood, approximately two thirds ofthe immune cells) have been identified, including inter­ circulating lymphocytes are T-cells, and one third are ferons, migration inhibiting factor (MIF), and transfer B-cells. Of the T-lymphocytes in the blood, approxi­ factor. mately two thirds are helper T-cells and one third suppressor T-cells, giving the "normal" helper-to- Monocyte-macrophages are involved in these pro­ suppressor ratio of approximately 1.2:2.2 in normal, cesses in at least two steps (7). Early on, these cells healthy adults (5). In other tissues, T-cells constitute encounter new antigens, "process" them, and present more than 75% of the lymphocytes in lymph and lymph them to wandering T- and B-cells. Once "activated" by nodes, and B-cells more than 75% of the lymphocytes in these antigens, the T- and B-cells undergo the changes the bone marrow. The proportion of T- and B- described earlier. Eventually, the lymphokines (eg, MIF lymphocytes in the spleen is approximately 50% of and others) released by these activated lymphocytes each. further influence the monocyte-macrophages to per­ form their effector functions in a more vigorous manner (turned on, "angry," activated macrophages). One such Immunologic Findings in AIDS specialized cell in the epidermis, the Langerhans cell, serves as the antigen-presenting cell in the skin. Other with Routine Screening Techniques types of these cells are found in important areas in the In view of the complexity of the immune system, the lymphoid tissues and organs. many tests available for use or abuse, and the need for accurate, timely, and cost-effective diagnostic tests in A review of the immune system organization requires patients at risk for AIDS, it is very important for clini­ more detailed mention of the chemical signals that cians to be aware of the office and laboratory clues that regulate cell growth and differentiation (8). A major can be readily obtained without a sophisticated immu­ lymphokine is interleukin-2, which was originally de nology laboratory. It should be reemphasized that AIDS scribed in the mid-1970s and named T-cell growth factor. is a syndrome; even with the most expensive tech­ Interleukin-2 is produced by T-cells, and it in turn stimu­ nology available today, the diagnosis cannot be made lates the division of T-cells. In addition, interleukin-2 with laboratory testing alone. stimulates T-cells to produce gamma (immune) inter­ Patients who meet the rigorous Centers for Disease feron which also serves as a lymphokine with several Control (CDC) criteria (2,3) for the diagnosis of AIDS defined important functions. Interleukin-2 seems to will almost invariably have evidence of cellular immu­ have a limited range of sources and targets. Only T-cells nodeficiency. Opportunistic infections with micro­ that are antigenically stimulated will respond to organisms (especially viral, fungal, mycobacterial, and interleukin-2. In contrast, interleukin-1 has a wide range parasitic) and/or the presence of certain tumors against of effects on non-lymphocytic cells which contribute to which cellular immunity (T-cell mediated
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