Editing Immunology (section)

== Developmental immunology ==

The body's capability to react to antigens depends on a person's age, antigen type, maternal factors and the area where the antigen is presented.<ref name="isbn0-7167-4947-5">{{cite book |vauthors=Goldsby RA, Kindt TK |author3=Osborne BA |author4=Kuby J |title=Immunology |edition=5th |publisher=W.H. Freeman |location=San Francisco |date=2003 |isbn=978-0-7167-4947-9 |url=https://archive.org/details/immunology00gold_0 }}</ref> [[Neonate]]s 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 [[glycoprotein]]s and [[polysaccharide]]s. In fact, many of the infections acquired by neonates are caused by low virulence organisms like ''[[Staphylococcus]]'' and ''[[Pseudomonas]]''.  In neonates, [[Opsonin|opsonic]] activity and the ability to activate the [[complement cascade]] is very limited.  For example, the mean level of [[Apolipoprotein C3<!--Is this correct?-->|C3]] in a newborn is approximately 65% of that found in the adult. [[Phagocytosis|Phagocytic]] activity is also greatly impaired in newborns. This is due to lower opsonic activity, as well as diminished [[Downregulation and upregulation|up-regulation]] of [[integrin]] and [[selectin]] receptors, which limit the ability of [[neutrophil]]s to interact with [[Cell adhesion molecule|adhesion molecule]]s in the [[endothelium]]. Their [[monocyte]]s are slow and have a reduced [[Adenosine triphosphate|ATP]] production, which also limits the newborn's phagocytic activity.  Although, the number of total [[lymphocyte]]s is significantly higher than in adults, the cellular and humoral immunity is also impaired. [[Antigen-presenting cell]]s in newborns have a reduced capability to activate T&nbsp;cells.  Also, T&nbsp;cells of a newborn proliferate poorly and produce very small amounts of [[cytokine]]s 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&nbsp;cells develop early during [[gestation]] but are not fully active.<ref name="Jaspan et al">{{cite journal | vauthors = Jaspan HB, Lawn SD, Safrit JT, Bekker LG | title = The maturing immune system: implications for development and testing HIV-1 vaccines for children and adolescents | journal = AIDS | volume = 20 | issue = 4 | pages = 483–94 | date = February 2006 | pmid = 16470112 | doi = 10.1097/01.aids.0000210602.40267.60 | s2cid = 20277590 | doi-access = free }}</ref>

[[File:Monocyte.svg|thumb|Artist's impression of [[monocyte]]s]]

Maternal factors also play a role in the body's immune response.  At birth, most of the [[immunoglobulin]] present is maternal IgG. These antibodies are transferred from the placenta to the fetus using the FcRn (neonatal Fc receptor).<ref>{{Cite web|url=https://www.immunology.org/public-information/bitesized-immunology/immune-development/neonatal-immunology|title=Neonatal Immunology &#124; British Society for Immunology|website=www.immunology.org}}</ref> Because IgM, IgD, IgE and IgA do not cross the placenta, they are almost undetectable at birth. Some IgA is provided by [[breast milk]]. These passively-acquired antibodies can protect the newborn for up to 18 months, but their response is usually short-lived and of low [[Affinity (pharmacology)<!--Is this correct?-->|affinity]].<ref name="Jaspan et al"/>  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. [[Passive immunity|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.<ref name="Jaspan et al"/> Between six and nine months after birth, a child's immune system begins to respond more strongly to [[glycoprotein]]s, but there is usually no marked improvement in their response to [[polysaccharide]]s until they are at least one year old. This can be the reason for distinct time frames found in [[vaccination schedule]]s.<!--
     --><ref name="pmid11739030">{{cite journal | vauthors = Glezen WP | title = Maternal vaccines | journal = Primary Care | volume = 28 | issue = 4 | pages = 791–806, vi–vii | date = December 2001 | pmid = 11739030 | doi = 10.1016/S0095-4543(05)70041-5 }}</ref><!--
     --><ref name="pmid9286377">{{cite book | vauthors = Holt PG, Macaubas C, Cooper D, Nelson DJ, McWilliam AS | chapter = Th-1/Th-2 Switch Regulation in Immune Responses to Inhaled Antigens | title = Dendritic Cells in Fundamental and Clinical Immunology | volume = 417 | pages = 301–06 | date = 1997 | pmid = 9286377 | doi = 10.1007/978-1-4757-9966-8_49 | isbn = 978-1-4757-9968-2 | series = Advances in Experimental Medicine and Biology }}</ref>

During adolescence, the human body undergoes various physical, physiological and immunological changes triggered and mediated by [[hormone]]s, of which the most significant in females is [[Estradiol|17-β-estradiol]] (an [[estrogen]]) and, in males, is [[testosterone]]. Estradiol usually begins to act around the age of 10 and testosterone some months later.<ref name="pmid127002">{{cite journal | vauthors = Sizonenko PC, Paunier L | title = 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 | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 41 | issue = 5 | pages = 894–904 | date = November 1975 | pmid = 127002 | doi = 10.1210/jcem-41-5-894 }}</ref> <!--
 -->There is evidence that these [[steroid]]s not only act directly on the [[Primary sexual characteristics|primary]] and [[secondary sexual characteristics]] but also have an effect on the development and regulation of the immune system,<ref name="pmid11407317">{{cite journal | vauthors = Verthelyi D | title = Sex hormones as immunomodulators in health and disease | journal = International Immunopharmacology | volume = 1 | issue = 6 | pages = 983–93 | date = June 2001 | pmid = 11407317 | doi = 10.1016/S1567-5769(01)00044-3 }}</ref> <!--
 -->including an increased risk in developing [[Puberty|pubescent]] and post-pubescent autoimmunity.<ref name="pmid2973658">{{cite journal | vauthors = Stimson WH | title = Oestrogen and human T lymphocytes: presence of specific receptors in the T-suppressor/cytotoxic subset | journal = Scandinavian Journal of Immunology | volume = 28 | issue = 3 | pages = 345–50 | date = September 1988 | pmid = 2973658 | doi = 10.1111/j.1365-3083.1988.tb01459.x | s2cid = 38920551 }}</ref> <!--
 -->There is also some evidence that cell surface receptors on B cells and macrophages may detect sex hormones in the system.<ref name="pmid11996938">{{cite journal | vauthors = Benten WP, Stephan C, Wunderlich F | title = B cells express intracellular but not surface receptors for testosterone and estradiol | journal = Steroids | volume = 67 | issue = 7 | pages = 647–54 | date = June 2002 | pmid = 11996938 | doi = 10.1016/S0039-128X(02)00013-2 | s2cid = 1056135 }}</ref>

The female sex hormone 17-β-estradiol has been shown to regulate the level of immunological response,<ref name="pmid12900050">{{cite journal | vauthors = Beagley KW, Gockel CM | title = Regulation of innate and adaptive immunity by the female sex hormones estradiol and progesterone | journal = FEMS Immunology and Medical Microbiology | volume = 38 | issue = 1 | pages = 13–22 | date = August 2003 | pmid = 12900050 | doi = 10.1016/S0928-8244(03)00202-5 | doi-access = free }}</ref> <!--
 -->while some male [[androgen]]s such as testosterone seem to suppress the stress response to infection. Other androgens, however, such as [[DHEA]], increase immune response.<ref name="pmid9949320">{{cite journal | vauthors = Kanda N, Tamaki K | title = Estrogen enhances immunoglobulin production by human PBMCs | journal = The Journal of Allergy and Clinical Immunology | volume = 103 | issue = 2 Pt 1 | pages = 282–88| date = February 1999 | pmid = 9949320 | doi = 10.1016/S0091-6749(99)70503-8 }}</ref> <!--
 -->As in females, the male sex hormones seem to have more control of the immune system during puberty and post-puberty than during the rest of a male's adult life.

Physical changes during puberty such as [[thymic involution]] also affect immunological response.<ref name="pmid10737767">{{cite journal | vauthors = McFarland RD, Douek DC, Koup RA, Picker LJ | title = Identification of a human recent thymic emigrant phenotype | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 97 | issue = 8 | pages = 4215–20 | date = April 2000 | pmid = 10737767 | pmc = 18202 | doi = 10.1073/pnas.070061597 | bibcode = 2000PNAS...97.4215M | doi-access = free }}</ref>