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74 SECTION I  Cellular and Molecular Basis for Medical Physiology

TABLE 3–2  Examples of cytokines and their clinical relevance.


Cytokine Cellular Sources Major Activities Clinical Relevance

Interleukin-1 Macrophages Activation of T cells and macrophages; Implicated in the pathogenesis of septic shock,
promotion of inflammation rheumatoid arthritis, and atherosclerosis
Interleukin-2 Type 1 (TH1) helper T cells Activation of lymphocytes, natural Used to induce lymphokine-activated killer cells;
killer cells, and macrophages used in the treatment of metastatic renal cell
carcinoma, melanoma, and various other tumors
Interleukin-4 Type 2 (TH2) helper T cells, Activation of lymphocytes, As a result of its ability to stimulate IgE
mast cells, basophils, and monocytes, and IgE class switching production, plays a part in mast-cell sensitization
eosinophils and thus in allergy and in defense against
nematode infections
Interleukin-5 Type 2 (TH2) helper T cells, Differentiation of eosinophils Monoclonal antibody against interleukin-5
mast cells, and eosinophils used to inhibit the antigen-induced late-phase
eosinophilia in animal models of allergy
Interleukin-6 Type 2 (TH2) helper T cells Activation of lymphocytes; Overproduced in Castleman disease; acts as
and macrophages differentiation of B cells; stimulation an autocrine growth factor in myeloma and in
of the production of acute-phase mesangial proliferative glomerulonephritis
proteins
Interleukin-8 T cells and macrophages Chemotaxis of neutrophils, basophils, Levels are increased in diseases accompanied
and T cells by neutrophilia, making it a potentially useful
marker of disease activity
Interleukin-11 Bone marrow stromal cells Stimulation of the production of Used to reduce chemotherapy-induced
acute-phase proteins thrombocytopenia
Interleukin-12 Macrophages and B cells Stimulation of the production of May be useful as an adjuvant for vaccines
inter-feron γ by type 1 (TH1) helper
T cells and by natural killer cells;
induction of type 1 (TH1) helper T cells
Interleukin-17 T cells Promotion of inflammatory cell Implicated in many immune/autoimmune
chemotaxis and inflammation diseases such as rheumatoid arthritis, asthma,
and psoriasis
Tumor necrosis Macrophages, natural Promotion of inflammation Treatment with antibodies against tumor
factor-α killer cells, T cells, B cells, necrosis factor-α beneficial in rheumatoid
and mast cells arthritis and Crohn disease
Lymphotoxin (tumor Type 1 (TH1) helper T cells Promotion of inflammation Implicated in the pathogenesis of multiple
necrosis factor-β) and B cells sclerosis and insulin-dependent diabetes
mellitus
Transforming T cells, macrophages, Immunosuppression May be useful therapeutic agent in multiple
growth factor-β B cells, and mast cells sclerosis and myasthenia gravis
Granulocyte- T cells, macrophages, Promotion of the growth of Used to reduce neutropenia after chemotherapy
macrophage colony- natural killer cells, and granulocytes and monocytes for tumors and in ganciclovir-treated patients
stimulating factor B cells with AIDS; used to stimulate cell production after
hematopoietic stem cell transplantation
Interferon-α Virally infected cells Induction of resistance of cells to viral Used to treat AIDS-related Kaposi sarcoma,
infection melanoma, chronic hepatitis B infection, and
chronic hepatitis C infection
Interferon-β Virally infected cells Induction of resistance of cells to viral Used to reduce the frequency and severity of
infection relapses in multiple sclerosis
Interferon-γ Type 1 (TH1) helper T cells Activation of macrophages; inhibition Used to enhance the killing of phagocytosed
and natural killer cells of type 2 (TH2) helper T cells bacteria in chronic granulomatous disease

Modified with permission from Delves PJ, Roitt IM: The immune system. First of two parts, N Engl J Med 2000; July 6:343(1):37–49.

pathogens. Other PRRs may be intracellular, such as the


so-called NOD proteins. One NOD protein, NOD2, has
ACQUIRED IMMUNITY
received attention as the product of a candidate gene lead- As noted previously, the key to acquired immunity is the abil-
ing to the intestinal inflammatory condition, Crohn disease ity of lymphocytes to produce antibodies (in the case of B
(Clinical Box 3–2). cells) or cell-surface receptors (in the case of T cells) that are

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