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Immunodeficiency States Relevant to Infection

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Immunodeficiency States Relevant to Infection Immunodeficiency states relevant to infection The importance of immune mechanisms in resistance to infection is most apparent in persons with deficient immunity. Although immuno- John D. Clough, M.D. deficiency states are relatively uncommon, the study of patients with such defects has led to Department of Rheumatic Disease significant insights into the functioning of the normal immune system. Moreover, from a practi- cal point of view, it is occasionally necessary to consider the differential diagnosis of immune deficiency in patients with repeated infections, or in patients with unusual infections. To approach an evaluation rationally, it is helpful to have some broad concepts about the organization of the immune system. This paper presents a simple review of the functional and morphologic organization of the immune system, a discussion of the differential diagnosis of immunodeficiency states, and an orderly approach to the examination of patients suspected of having immune deficiency. Organization of the immune system Since the early work of Miller1 in clarifying the role of the thymus gland and that of Cooper et al2 in defining the function of the bursa of Fabricius in chickens, the binary structure of the immune system has become widely accepted. Primordial immunocytes from bone marrow mature along one of two pathways under the in- fluence of the two central lymphoid organs, the thymus gland and the bursa or bursal equivalent (.Fig.l). 49 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. 50 Cleveland Clinic Quarterly Vol. 42, No. 1 ® IMMUNE SYSTEM Fig. 1. Organization of the immune system. Numbers refer to presumed defect sites and corre- spond to numbered paragraphs in the text. (Adapted from Cleve Clin Q41: 128, 1974.) The thymic influence leads to gen- jection,7 graft versus host reactions,8 eration of the T-cell population, which and probably play an important role includes the great majority of cells in in tumor surveillance.9 Adequate T- the thymus gland itself, cells in the cell function is crucial in the defense "thymic-dependent" areas of periph- against infection by intracellular para- eral lymph nodes (paracortical areas), sites such as mycobacteria, brucella, and a circulating population of small many viruses, and Pneumocystis lymphocytes found in the blood and carinii. 3 lymphatic vessels. Although it is not A number of tests of T-cell function clear how many distinguishable sub- are available including delayed hyper- populations of T-cells exist or how the sensitivity skin tests, mitogen- or anti- various functions are parceled out gen-induced lymphocyte transforma- among them, recirculating mature T- tion, migration inhibition factor cells, perhaps comparable to T-2 cells (MIF) production, mixed lymphocyte 4 in mice, tend to be long-lived; their reactions, and in vitro cytotoxicity numbers are not greatly affected by (especially relevant in tumor immu- thymectomy, but because they recircu- nity). T-cells in circulation can be 5 late, they can be depleted rapidly by directly quantitated by taking advan- thoracic duct drainage, and are maxi- tage of their ability to form rosettes mally accessible to antilymphocyte with sheep erythrocytes;10 normally, serum. These cells are responsible for approximately 70% of peripheral 6 delayed hypersensitivity, allograft re- blood lymphocytes are T-cells. Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. Spring 1975 Immunodeficiency states relevant to infection 51 Immunocytes maturing under the about 30% of peripheral blood lym- influence of the bursa or bursal equiv- phocytes are B-cells. alent constitute the B-cell population, These two populations of cells give which includes most of the cells found rise to cell-mediated and humoral in the bursa of Fabricius of birds, the immune responses when triggered by cells found in the "bursal-dependent" appropriate antigenic stimuli. The areas of lymph nodes (germinal centers outcome of such responses depends on and far cortical areas), plasma cells, the activation of a wide variety of effec- and a population of circulating lym- tor mechanisms. Effector mechanisms phocytes.3 B-cells do not recirculate as are, by and large, without specificity. extensively as T-cells and their life When they are activated immuno- span is much shorter than that of T- logically, their destructive effects are cells.4 The major function of the B- ordinarily brought to bear against the cell system is antibody production. specific stimulating agent, although Antibody activity is borne by proteins this may not always be the case. It called immunoglobulins, which are should also be kept in mind that some separable by antigenic, physical, and of these effector mechanisms may be functional characteristics into five dis- activated by nonimmunologic path- tinct classes: IgM, IgG, IgA, IgD, and ways. IgE. IgM and IgG are the major cir- When an immunogenic material en- culating immunoglobulins, the former ters the system, it eventually finds its dominating primary immune re- way (sometimes after "antigen-process- sponses and responses to polysaccha- ing" by macrophages) to appropriate ride antigens, the latter dominating antigen-sensitive T- or B-cells or both. secondary responses to protein anti- The immunogen interacts with surface 11 gens. IgA is the major immunoglobu- receptors on these cells, and in this 12 lin of exocrine secretions, although way the antigen-sensitive cells are it is also found in the circulation. IgE triggered, initiating the immune re- 13 is largely tissue-fixed, and only a sponse. At this point, interactions may small amount is present in the circula- occur between the stimulated T- and tion. IgD is to a large extent bound to B-cells which lead either to enhance- B-cells and may play a role in induc- ment18 or suppression19 of the re- 14 tion of the immune response. Anti- sponse. Activation of such antigen- bodies are important in resistance to sensitive cells has several results. In pyogenic bacterial infections and some both T- and B-cell systems prolifera- viral infections. tion occurs, and this produces a much B-cell function is assessed by mea- larger population of specific antigen- suring immunoglobulin levels and sensitive cells establishing immuno- antibody responses. Circulating B-cells logic memory. In the T-cell system, can be enumerated by staining lym- both by proliferation and recruitment, phocytes with fluorescein-tagged anti- a population of cells is produced globulins,15 by rosette formation with which launches a direct attack on the sensitized sheep erythrocytes bear- immunogen itself. In the B-cell sys- ing complement components through tem, the antibody production mecha- C3,16 or by binding of fluorescein- nism is activated, resulting in the pro- tagged aggregated IgG.17 Normally duction of various classes of immuno- Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. 52 Cleveland Clinic Quarterly Vol. 42, No. 1 globulins which specifically combine classical and alternate pathways may with the antigen, and produce com- on occasion be activated by nonim- plexes which can activate several effec- mune mechanisms. Activation of C3 tor mechanisms. to C3b leads to a positive feedback Effectors of humoral immunity. Al- mechanism which utilizes some of the though the mere combination of anti- components of the alternate pathway body with antigen may alter the anti- in activating further molecules of C3. gen in various ways, it generally does The potent biological effects of com- not result in destruction or rapid plement begin with C3 activation. The elimination of antigen from the body. fixation of C3b leads to opsonization Auxiliary mechanisms must be acti- for phagocytosis of many antigens in- vated to accomplish this. The best cluding most gram-positive bacteria. understood of these auxiliary mecha- The subsequent activation of C5 leads nisms is the complement system. to further opsonization and is required Complement is the effector system for phagocytosis of many gram-nega- for antibodies in the major immuno- tive bacteria and Staphylococcus globulin classes; IgG and IgM anti- aureus as well as many fungi. Ana- bodies activate the classical path- phylotoxins (C3a and C5a) are re- way,20 and IgA antibodies may activate leased with activation of the third and the alternate pathway.21 Current data fifth components. Chemotaxis of indicate that antibodies of the other phagocytes is produced by activation classes (IgD and IgE) are unable to of C5, C6, and C7 with C567 complex activate the complement cascade, al- formation. If the antigen is on a cell though there is some evidence to sug- surface, activation of C8 and C9 pro- gest that IgE may activate the alter- duces damage at the antigenic site nate pathway.22 The complement which may result in lysis of the cell. system is a group of alpha, beta, and The complement system, then, is im- gamma globulins with potential en- portant in mediating the destruction zymatic activity, which are activated of antigen and its elimination from the sequentially in a fashion analogous to system. Its complexity, together with the coagulation mechanism. Their the presence of inhibitors at several relationships are shown in Figure 2. steps, help to protect the host against The pivotal step in the cascade is acti- self-infliction of damage by inappro- vation of the third component of com- priate activation of
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