The first signal is provided by antigenic peptides displayed in MHC molecules. The second is provided by one or more costimulatory molecule produced by the antigen-presenting cell, in response to molecules displayed by pathogens. If these costimulatory signaling molecules are not present, the T cell-MHC interaction may alternatively cause the T cell to undergo programmed cell death, a process known as apoptosis.

Reference: Paul WE (ed): Fundamental Immunology, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2003.

Cell-mediated immunity involves the action of T cells. CD8+ cytolytic T cells can kill target cells directly. CD4+ helper cells can activate macrophages to become more effective at killing the organisms they ingest. This process is also considered to be cell-mediated immunity, although, again, a cell of the innate system carries out the ultimate effector function. Cells of the innate system are also needed to initiate humoral and cell-mediated responses. Dendritic cells and macrophages ingest organisms, digest them into peptides, and present them to T cells and B cells in a way that causes antigen-specific lymphocytes to proliferate and differentiate into effector cells.

Reference: Paul WE (ed): Fundamental Immunology, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2003.

Humoral immunity involves antibodies, produced by B cells. Terminally differentiated B cells, called plasma cells, produce most of the antibodies. Humoral immune responses defend the host against extracellular bacteria and toxins. Blocking antibodies can prevent the adherence of bacteria, viruses, or toxins to host cells. Antibodies can activate complement through the classical pathway and lyse cells. Complement activation also generates chemotactic fragments that activate mast cells and phagocytes and chemotactically attract phagocytic cells into sites of inflammation. NK cells can bind to antibody-coated targets and lyse them in antibody-mediated cytotoxicity. Antibodies can also opsonize; in other words, their binding facilitates uptake of the antigen by phagocytic cells.

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The disadvantage of the adaptive immunes response is that the required expansion process takes time after the first encounter with antigen, in some cases more than 2 weeks. Many infectious agents can cause death or severe disability in less time than it takes the adaptive immune system to mobilize a specific response. This disadvantage leaves a gap in the host defense system.

Reference:  Abbas AK, Lichtman AH: Cellular and Molecular Immunology, 5th ed. Philadelphia, W.B. Saunders, 2003.

The distinct advantage of the adaptive immune system is its ability to select B cells and T cells that have high-affinity receptors for new antigens and to stimulate them to replicate and provide a specific, fine-tuned response to foreign invaders.

Reference:  Abbas AK, Lichtman AH: Cellular and Molecular Immunology, 5th ed. Philadelphia, W.B. Saunders, 2003.

The adaptive immune system includes elements such as the B lymphocytes that make antibodies and T lymphocytes that provide the effector elements of antigen-specific cell-mediated immune responses. Elements of the adaptive immune system display a large repertoire (e.g., tens of millions) of specific antigen receptors that are generated by DNA rearrangements. Each lymphocyte and its clonal descendants express one of the millions of possible antigen receptors. Since numerically there are very few cells at any one time that can recognize newly introduced antigens, B cells and T cells must be appropriately stimulated and induced to divide and produce multiple copies of themselves.

Reference:  Klein J: Immunology, 2nd ed. Oxford, Blackwell Scientific Publications, 1997.

Neutrophils, monocytes, macrophages, eosinophils, basophils, mast cells, natural killer (NK) cells, complement proteins, and acute-phase reactants. All of these elements have germline-encoded receptors that recognize motifs commonly present on microbes.

Reference:  Rich RR, Fleisher TA, Shearer WT, et al: Clinical Immunology, Principles and Practice, 2nd ed. St. Louis, Mosby, 2001.

Innate immunity is the first line of defense against infection because its elements are already present in the circulation and can respond immediately to microbial invasion. However, the innate system has no memory; on subsequent exposure to the same antigen, the response is no greater, no faster, and no more effective than it was on first exposure to antigen.

Reference:  Adkinson NF, Yunginger A, Busse W, et al (eds): Middleton’s Allergy: Principles and Practice, 6th ed. St. Louis, Mosby, 2004.

The immune system can be considered to have two major divisions: the innate immune system and the adaptive or cognitive immune system. The innate immune system is phylogenetically older.

Reference: Adkinson NF, Yunginger A, Busse W, et al (eds): Middleton’s Allergy: Principles and Practice, 6th ed. St. Louis, Mosby, 2004.

Glutamine-enriched enteral nutrition in very low-birth-weight infants decreased the incidence of atopic dermatitis during the first year of life but had no effect on the incidence of bronchial hyperreactivity and infectious diseases during the first year of life.

The authors determined the effect of glutamine-enriched enteral nutrition in very low-birth-weight infants on the incidence of allergic and infectious diseases during the first year of life. They did a follow-up study in a tertiary care hospital. Participants are all surviving infants who participated in a trial of glutamine-enriched enteral nutrition in very low-birth-weight infants. They give enteral glutamine supplementation (l-glutamine, 0.3 g/kg per day) from 3 through 30 days of life. They observed the incidence of allergic and infectious diseases during the first year of life, as assessed by means of validated questionnaires. Seventy-seven of 90 infants (86%) participated in the follow-up study. Baseline patient, maternal, and environmental characteristics did not differ between the glutamine-supplemented (n = 37) and control (n = 40) groups, except for the incidence of serious neonatal infections and child care attendance. After adjustment for confounding factors, the risk for atopic dermatitis was lower in the glutamine-supplemented group (odds ratio [OR], 0.13; 95% confidence interval [CI], 0.02-0.97). However, the incidence of bronchial hyperreactivity (OR, 0.34; 95% CI, 0.10-1.21) and infections of the upper respiratory (OR, 0.99; 95% CI, 0.35-2.79), lower respiratory (OR, 0.39; 95% CI, 0.13-1.24), and gastrointestinal (OR 1.25, 95% CI 0.23-6.86) tracts was not different between the treatment groups.

Reference: Arch Pediatr Adolesc Med. 2007 Nov;161(11):1095-101