Basic Lecture of Immunology

The body’s capability to react to antigen depends on a person’s age, antigen type, maternal factors and the area where the antigen is presented.[2] Neonates are said to be in a state of physiological immunodeficiency, because both their innate and adaptive immunological responses are greatly suppressed. Once born, a child’s immune system responds favorably to protein antigens while not as well to glycoproteins and polysaccharides. In fact, many of the infections acquired by neonates are caused by low virulence organisms like Staphylococcus and Pseudomonas. In neonates, opsonic activity and the ability to activate the complement cascade is very limited. For example, the mean level of C3 in a newborn is approximately 65% of that found in the adult. Phagocytic activity is also greatly impaired in newborns. This is due to lower opsonic activity, as well as diminished up-regulation of integrin and selectin receptors, which limit the ability of neutrophils to interact with adhesion molecules in the endothelium. Their monocytes are slow and have a reduced ATP production, which also limits the newborns phagocytic activity. Although, the number of total lymphocytes is significantly higher than in adults, the cellular and humoral immunity is also impaired. Antigen presenting cells in newborns have a reduced capability to activate T cells. Also, T cells of a newborn proliferate poorly and produce very small amounts of cytokines like IL-2, IL-4, IL-5, IL-12, and IFN-g which limits their capacity to activate the humoral response as well as the phagocitic activity of macrophage. B cells develop early in gestation but are not fully active.[3]

Monocytes: An Artist’s Impression

Maternal factors also play a role in the body’s immune response. At birth most of the immunoglobulin is present is maternal IgG. Because IgM, IgD, IgE and IgA don’t cross the placenta, they are almost undetectable at birth. Although some IgA is provided in breast milk. These passively acquired antibodies can protect the newborn up to 18 months, but their response is usually short-lived and of low affinity.[3] These antibodies can also produce a negative response. If a child is exposed to the antibody for a particular antigen before being exposed to the antigen itself then the child will produce a dampened response. Passively acquired maternal antibodies can suppress the antibody response to active immunization. Similarly the response of T-cells to vaccination differs in children compared to adults, and vaccines that induce Th1 responses in adults do not readily elicit these same responses in neonates.[3] By 6-9 months after birth, a child’s immune system begins to respond more strongly to glycoproteins. Not until 12-24 months of age is there a marked improvement in the body’s response to polysaccharides. This can be the reason for the specific time frames found in vaccination schedules.[4][5]

During adolescence the human body undergoes several physical, physiological and immunological changes. These changes are started and mediated by different hormones. Depending on the sex either testosterone or 17-β-oestradiol, act on male and female bodies accordingly, start acting at ages of 12 and 10 years.[6]

There is evidence that these steroids act directly not only on the primary and secondary sexual characteristics, but also have an effect on the development and regulation of the immune system.[7]

There is an increased risk in developing autoimmunity for pubescent and post pubescent females and males.[8] There is also some evidence that cell surface receptors on B cells and macrophages may detect sex hormones in the system.[9]

The female sex hormone 17-β-oestradiol has been shown to regulate the level of immunological response.[10] Similarly, some male androgens, like testosterone, seem to suppress the stress response to infection; but other androgens like DHEA have the opposite effect, as it increases the immune response instead of down playing it.[11] As in females, the male sex hormones seem to have more control of the immune system during puberty and the time right after than in fully developed adults. Other than hormonal changes physical changes like the involution of the Thymus during puberty will also affect the immunological response of the subject or patient.[12]

Basic Lecture of Immunology are

1. ab-ag structure and interaction ok 11

2, Lect S2- immun Ig, switch, genetic Ig

3, immunotherapy-Immunology_mAb

4. imun respon to virus

Reference:

  1. ^ Janeway’s Immunobiology textbook Searchable free online version at the National Center for Biotechnology Information
  2. ^ Goldsby RA, Kindt TK, Osborne BA and Kuby J (2003). Immunology (5th ed.). San Francisco: W.H. Freeman. ISBN 0-7167-4947-5.
  3. ^ a b c Jaspan HB, Lawn SD, Safrit JT, Bekker LG (February 2006). “The maturing immune system: implications for development and testing HIV-1 vaccines for children and adolescents”. AIDS 20 (4): 483–94. doi:10.1097/01.aids.0000210602.40267.60. PMID 16470112.
  4. ^ Glezen WP (December 2001). “Maternal vaccines”. Prim. Care 28 (4): 791–806, vi–vii. doi:10.1016/S0095-4543(05)70041-5. PMID 11739030.
  5. ^ Holt PG, Macaubas C, Cooper D, Nelson DJ, McWilliam AS (1997). “Th-1/Th-2 switch regulation in immune responses to inhaled antigens. Role of dendritic cells in the aetiology of allergic respiratory disease”. Adv. Exp. Med. Biol. 417: 301–6. PMID 9286377.
  6. ^ Sizonenko PC, Paunier L (November 1975). “Hormonal changes in puberty III: Correlation of plasma dehydroepiandrosterone, testosterone, FSH, and LH with stages of puberty and bone age in normal boys and girls and in patients with Addison’s disease or hypogonadism or with premature or late adrenarche”. J. Clin. Endocrinol. Metab. 41 (5): 894–904. doi:10.1210/jcem-41-5-894. PMID 127002.
  7. ^ Verthelyi D (June 2001). “Sex hormones as immunomodulators in health and disease”. Int. Immunopharmacol. 1 (6): 983–93. doi:10.1016/S1567-5769(01)00044-3. PMID 11407317.
  8. ^ Stimson WH (September 1988). “Oestrogen and human T lymphocytes: presence of specific receptors in the T-suppressor/cytotoxic subset”. Scand. J. Immunol. 28 (3): 345–50. doi:10.1111/j.1365-3083.1988.tb01459.x. PMID 2973658.
  9. ^ Benten WP, Stephan C, Wunderlich F (June 2002). “B cells express intracellular but not surface receptors for testosterone and estradiol”. Steroids 67 (7): 647–54. doi:10.1016/S0039-128X(02)00013-2. PMID 11996938.
  10. ^ Beagley KW, Gockel CM (August 2003). “Regulation of innate and adaptive immunity by the female sex hormones oestradiol and progesterone”. FEMS Immunol. Med. Microbiol. 38 (1): 13–22. doi:10.1016/S0928-8244(03)00202-5. PMID 12900050.
  11. ^ Kanda N, Tamaki K (February 1999). “Estrogen enhances immunoglobulin production by human PBMCs”. J. Allergy Clin. Immunol. 103 (2 Pt 1): 282–8. doi:10.1016/S0091-6749(99)70503-8. PMID 9949320.
  12. ^ McFarland RD, Douek DC, Koup RA, Picker LJ (April 2000). “Identification of a human recent thymic emigrant phenotype”. Proc. Natl. Acad. Sci. U.S.A. 97 (8): 4215–20. doi:10.1073/pnas.070061597. PMC 18202. PMID 10737767.
  13. ^ Miller JJ, Valdes R (February 1991). “Approaches to minimizing interference by cross-reacting molecules in immunoassays”. Clin. Chem. 37 (2): 144–53. PMID 1993317.
  14. ^ “Office of Science Education – LifeWorks – Immunologist”. Retrieved 2009-09-10.
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