Immunology basics - Revision history

wikademia>Eme: /* External links */

2014-06-17T05:27:28Z

External links

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	== External links ==		== External links ==
	~~{{WVD}}~~
	* [http://www.dayofimmunology.org/ April the 29th - the annual Day of Immunology]		* [http://www.dayofimmunology.org/ April the 29th - the annual Day of Immunology]
	* [[Annual Review of Immunology]] ([http://arjournals.annualreviews.org/loi/immunol journal home])		* [[Annual Review of Immunology]] ([http://arjournals.annualreviews.org/loi/immunol journal home])

wikademia>Wikademia at 06:22, 13 June 2009

2009-06-13T06:22:28Z

← Older revision		Revision as of 06:22, 13 June 2009
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	'''Immunology''' is a broad branch of [[biomedical science\|biomedical]] [[science]] that covers the study of all aspects of the [[immune system]] in all [[organism]]s. It deals with, among other things, the [[physiology\|physiological]] functioning of the immune system in states of both health and disease; malfunctions of the immune system in immunological disorders ([[autoimmune diseases]], [[hypersensitivity\|hypersensitivities]], [[immune deficiency]], [[transplant rejection]]); the physical, chemical and physiological characteristics of the components of the immune system [[in vitro]], [[in situ]], and [[in vivo]]. Immunology has applications in several disciplines of science, and as such is further divided.		'''Immunology''' is a broad branch of [[biomedical science\|biomedical]] [[science]] that covers the study of all aspects of the [[immune system]] in all [[organism]]s. It deals with, among other things, the [[physiology\|physiological]] functioning of the immune system in states of both health and disease; malfunctions of the immune system in immunological disorders ([[autoimmune diseases]], [[hypersensitivity\|hypersensitivities]], [[immune deficiency]], [[transplant rejection]]); the physical, chemical and physiological characteristics of the components of the immune system [[in vitro]], [[in situ]], and [[in vivo]]. Immunology has applications in several disciplines of science, and as such is further divided.
			{{?}}
	==Histological examination of the immune system==		==Histological examination of the immune system==
	Even before the concept of [[immunity (medical)\|immunity]] (from ''immunis'', Latin for "exempt") was developed, numerous early physicians characterized organs that would later prove to be part of the immune system. The key primary lymphoid organs of the immune system are [[thymus]] and [[bone marrow]], and secondary lymphatic tissues such as [[spleen]], [[tonsil]]s, [[lymphatic system\|lymph vessels]], [[lymph node]]s, [[adenoid]]s, and [[skin]]. When health conditions warrant, immune system organs including the thymus, spleen, portions of bone marrow, lymph nodes and secondary lymphatic tissues can be [[surgery\|surgically]] excised for examination while patients are still alive.		Even before the concept of [[immunity (medical)\|immunity]] (from ''immunis'', Latin for "exempt") was developed, numerous early physicians characterized organs that would later prove to be part of the immune system. The key primary lymphoid organs of the immune system are [[thymus]] and [[bone marrow]], and secondary lymphatic tissues such as [[spleen]], [[tonsil]]s, [[lymphatic system\|lymph vessels]], [[lymph node]]s, [[adenoid]]s, and [[skin]]. When health conditions warrant, immune system organs including the thymus, spleen, portions of bone marrow, lymph nodes and secondary lymphatic tissues can be [[surgery\|surgically]] excised for examination while patients are still alive.

wikademia>Wikademia at 06:22, 13 June 2009

2009-06-13T06:22:07Z

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 * [http://www.ibio.co.il/Products.aspx?level=2&prodID=26 Immunology products]
 [[Category:Immunology| ]]
 [[Category:Subjects taught in medical school]]

wikademia>Wikademia: moved Immunology to Immunology basics

2009-06-08T18:19:38Z

moved Immunology to Immunology basics

← Older revision	Revision as of 18:19, 8 June 2009
(No difference)

wikademia>Wikademia: 340 revisions

2009-06-08T18:18:48Z

340 revisions

← Older revision	Revision as of 18:18, 8 June 2009
(No difference)

129.107.62.86: /* Developmental Immmunology */

2009-06-02T16:04:18Z

Developmental Immmunology

← Older revision		Revision as of 16:04, 2 June 2009
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	==Developmental Immmunology==		==Developmental Immmunology==

	Adolescence is the age or biological time at which the human body start to develop from an infantile form to a fully-grown adult. During this time several physical, physiological and immunological changes start to occur inside the developing human body. 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 (2). There is evidence that these steroids act directly not only the primary and secondary sexual ~~characteristic~~ but also have an effect on the development and regulation of the immune system (3). There is ~~and increase~~ risk in developing autoimmunity for ~~pubertal~~ and post ~~pubertal~~ females and males (4). There ~~are~~ also evidence of cell surface receptors on T cells and Macrophages that detect sex hormones in the system (5). The female sex hormone 17-β-oestradiol has been shown to regulate de level of immunological response (6). For example ~~during the follicular phase of the menstrual cycle~~ there is a greater drop of IgG than ~~that~~ of IgA in adolescent females ~~that in adult ones~~ also other immune cells like macrophages and APC cells seem to ~~response~~ to this fluctuation of 17-β-oestradiol specifically in the mucosal layer on the womb of post ~~puberty~~ females (7). It has been suggested that this level of control is achieved by the stimulation of peripheral blood monocytes cells (PBMC) by 17-β-oestradiol (7). ~~On the~~ male androgens, like testosterone ~~seems~~ to suppress the stress response to infection; but other androgens like DHEA have the opposite effect ~~of testosterone~~ as it increases the immune response instead of down playing it (8). 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 (9). These differences occurring not only during development but also in sex hormones makes the development of vaccines or antitoxins extra challenging for the immunologist because it simply presents more variables to take into account at the time of designing and testing new treatment and vaccines (8)[[File:DHEA.png\|thumb\|The structure of DHEA]]		Adolescence is the age or biological time at which the human body start to develop from an infantile form to a fully-grown adult. During this time several physical, physiological and immunological changes start to occur inside the developing human body. 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 (2). 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 (3). There is an increased risk in developing autoimmunity for pubescent and post pubescent females and males (4). There is also evidence of cell surface receptors on T cells and Macrophages that detect sex hormones in the system (5). The female sex hormone 17-β-oestradiol has been shown to regulate the level of immunological response (6). For example, compared to adult females, there is a greater drop in IgG levels than in those of IgA during the follicular phase of the menstrual cycle in adolescent females; also, other immune cells, like macrophages and APC cells, seem to respond to this fluctuation of 17-β-oestradiol, specifically in the mucosal layer on the womb of post pubescent females (7). It has been suggested that this level of control is achieved by the stimulation of peripheral blood monocytes cells (PBMC) by 17-β-oestradiol (7). 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 (8). 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 (9). These differences occurring not only during development but also in sex hormones makes the development of vaccines or antitoxins extra challenging for the immunologist because it simply presents more variables to take into account at the time of designing and testing new treatment and vaccines (8)[[File:DHEA.png\|thumb\|The structure of DHEA]]

	Neonates are said to be in a state of physiological immunodeficiency, because both, their innate and adaptive immunological responses are greatly ~~suppress~~. In fact, many of the infections they acquire are ~~cause~~ 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. ~~The phagocitic~~ activity is also greatly impaired in newborns. This is not only due to ~~a decrease in the~~ opsonic activity, but mainly, to a diminished up regulation of ~~integrins~~ and ~~selectins~~ 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 phagocitic activity. Although, the number of total lymphocytes is significantly higher than in adults, the cellular and humoral immunity is also impair. Antigen presenting cells in newborns have a reduced capability to activate T cells. Also, T cells of a newborn proliferate poorly and produce very little amount, if any, 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 no fully active. 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. By breast feeding the mother provides the newborn with some IgA. The passively acquired antibodies can protect the newborn up to 18 months, but their response is usually short-live and of low affinity (1). [[File:Monocyte.png\|thumb\|Monocytes: An Artists Impression]]		Neonates are said to be in a state of physiological immunodeficiency, because both their innate and adaptive immunological responses are greatly suppressed. In fact, many of the infections they acquire 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 not only due to lower opsonic activity, but mainly to a 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 phagocitic activity. Although, the number of total lymphocytes is significantly higher than in adults, the cellular and humoral immunity is also impair. Antigen presenting cells in newborns have a reduced capability to activate T cells. Also, T cells of a newborn proliferate poorly and produce very little amount, if any, 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 no fully active. 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. By breast feeding the mother provides the newborn with some IgA. The passively acquired antibodies can protect the newborn up to 18 months, but their response is usually short-live and of low affinity (1). [[File:Monocyte.png\|thumb\|Monocytes: An Artists Impression]]

	The body’s capability to react to antigen depends according to age (of the person), antigen type, maternal factors and the area where the antigen is presented.		The body’s capability to react to antigen depends according to age (of the person), antigen type, maternal factors and the area where the antigen is presented.

129.107.62.86: /* Developmental Immmunology */

2009-06-02T15:51:16Z

Developmental Immmunology

Show changes

wikademia>Wikademia at 13:30, 24 May 2009

2009-05-24T13:30:45Z

← Older revision		Revision as of 13:30, 24 May 2009
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	* [[Immunology]]		* [[Immunology]]
			* [[Immune response in central nervous system]]
	* [http://wikademia.org/Special:Search?search={{PAGENAME}}&fulltext=Search Search]		* [http://wikademia.org/Special:Search?search={{PAGENAME}}&fulltext=Search Search]

wikademia>Wikademia: Created page with '{{subst:Topic}}'

2009-05-24T13:30:33Z

Created page with '{{subst:Topic}}'

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118.92.132.79: Formated the images properly :)

2009-05-24T10:38:24Z

Formated the images properly :)

← Older revision		Revision as of 10:38, 24 May 2009
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	==Developmental Immmunology==		==Developmental Immmunology==

	Adolescence is the age or biological time at which the human body start to develop from an infantile form to a fully-grown adult. During this time several; physical, physiological and immunological changes start to occur inside the developing human body. 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 (2). There is evidence that these steroids act directly not only the primary and secondary sexual characteristic but also have an effect on the development and regulation of the immune system (3). There is and increase risk in developing autoimmunity for pubertal and post pubertal females and males (4). There are also evidence of cell surface receptors on T cells and Macrophages that detect sex hormones in the system (5). The female sex hormone 17-β-oestradiol has been shown to regulate de level of immunological response (6). For example during the follicular phase of the menstrual cycle there is a greater drop of IgG than that of IgA in adolescent females that in adult ones also other immune cells like macrophages and APC cells seem to response to this fluctuation of 17-β-oestradiol specifically in the mucosal layer on the womb of post puberty females (7). It has been suggested that this level of control is achieved by the stimulation of peripheral blood monocytes cells (PBMC) by 17-β-oestradiol (7). On the male androgens, like testosterone seems to suppress the stress response to infection; but other androgens like DHEA have the opposite effect of testosterone as it increases the immune response instead of down playing it (8). 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 (9). These differences occurring not only during development but also in sex hormones makes the development of vaccines or antitoxins extra challenging for the immunologist because it simply presents more variables to take into account at the time of designing and testing new treatment and vaccines (8)[[File:DHEA.png]]		Adolescence is the age or biological time at which the human body start to develop from an infantile form to a fully-grown adult. During this time several; physical, physiological and immunological changes start to occur inside the developing human body. 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 (2). There is evidence that these steroids act directly not only the primary and secondary sexual characteristic but also have an effect on the development and regulation of the immune system (3). There is and increase risk in developing autoimmunity for pubertal and post pubertal females and males (4). There are also evidence of cell surface receptors on T cells and Macrophages that detect sex hormones in the system (5). The female sex hormone 17-β-oestradiol has been shown to regulate de level of immunological response (6). For example during the follicular phase of the menstrual cycle there is a greater drop of IgG than that of IgA in adolescent females that in adult ones also other immune cells like macrophages and APC cells seem to response to this fluctuation of 17-β-oestradiol specifically in the mucosal layer on the womb of post puberty females (7). It has been suggested that this level of control is achieved by the stimulation of peripheral blood monocytes cells (PBMC) by 17-β-oestradiol (7). On the male androgens, like testosterone seems to suppress the stress response to infection; but other androgens like DHEA have the opposite effect of testosterone as it increases the immune response instead of down playing it (8). 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 (9). These differences occurring not only during development but also in sex hormones makes the development of vaccines or antitoxins extra challenging for the immunologist because it simply presents more variables to take into account at the time of designing and testing new treatment and vaccines (8)[[File:DHEA.png\|thumb\|The structure of DHEA]]

	Neonates are said to be in a state of physiological immunodeficiency, because both, their innate and adaptive immunological responses are greatly suppress. In fact, many of the infections they acquire are cause 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. The phagocitic activity is also greatly impaired in newborns. This is not only due to a decrease in the opsonic activity, but mainly, to a diminished up regulation of integrins and selectins 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 phagocitic activity. Although, the number of total lymphocytes is significantly higher than in adults, the cellular and humoral immunity is also impair. Antigen presenting cells in newborns have a reduced capability to activate T cells. Also, T cells of a newborn proliferate poorly and produce very little amount, if any, 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 no fully active. 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. By breast feeding the mother provides the newborn with some IgA. The passively acquired antibodies can protect the newborn up to 18 months, but their response is usually short-live and of low affinity (1). [[File:Monocyte.png]]		Neonates are said to be in a state of physiological immunodeficiency, because both, their innate and adaptive immunological responses are greatly suppress. In fact, many of the infections they acquire are cause 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. The phagocitic activity is also greatly impaired in newborns. This is not only due to a decrease in the opsonic activity, but mainly, to a diminished up regulation of integrins and selectins 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 phagocitic activity. Although, the number of total lymphocytes is significantly higher than in adults, the cellular and humoral immunity is also impair. Antigen presenting cells in newborns have a reduced capability to activate T cells. Also, T cells of a newborn proliferate poorly and produce very little amount, if any, 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 no fully active. 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. By breast feeding the mother provides the newborn with some IgA. The passively acquired antibodies can protect the newborn up to 18 months, but their response is usually short-live and of low affinity (1). [[File:Monocyte.png\|thumb\|Monocytes: An Artists Impression]]

	The body’s capability to react to antigen depends according to age (of the person), antigen type, maternal factors and the area where the antigen is presented.		The body’s capability to react to antigen depends according to age (of the person), antigen type, maternal factors and the area where the antigen is presented.