جفت
پاسخ : جفت
می گم یه سوالی که یه مدت پیش برام پیش اومده بود این بود که کورتیزول ترجیحی در شکستن پروتیئن ها برای گلوکونئوژنز دارد یا نه !!! مثلا اول سراغ انتی بادی نرود و یا سراغ dna پلی مراز نره ! این طوری می شه سیستم ایمنی هم ضعیف نشه (البته تضعیف سیستم ایمنی به دلیل لکوترین و پروستاگلندین و ..... هم هست ( افزایش یا کاهش ترشح بعضی از آن ها ))
می گم یه سوالی که یه مدت پیش برام پیش اومده بود این بود که کورتیزول ترجیحی در شکستن پروتیئن ها برای گلوکونئوژنز دارد یا نه !!! مثلا اول سراغ انتی بادی نرود و یا سراغ dna پلی مراز نره ! این طوری می شه سیستم ایمنی هم ضعیف نشه (البته تضعیف سیستم ایمنی به دلیل لکوترین و پروستاگلندین و ..... هم هست ( افزایش یا کاهش ترشح بعضی از آن ها ))
پاسخ : جفت
منبع : janeway immunology 8th ed
Tissue grafts placed in some sites in the body do not elicit immune responses.
For instance, the brain and the anterior chamber of the eye are sites in which
tissues can be grafed without inducing rejection. Such locations are termed
immunologically privileged sites (Fig. 15.7). It was originally believed that
immunological privilege arose from the failure of antigens to leave privileged
sites and induce immune responses. Subsequent studies have shown that
antigens do leave these sites and that they do interact with T cells. Instead of
eliciting a destructive immune response, however, they induce tolerance or a
response that is not destructive to the tissue.
Immunologically privileged sites are: brain - eye -testis -uterus -hamster cheek pouch
Immunologically privileged sites seem to be unusual in three ways. First, the
communication between the privileged site and the body is atypical in that
extracellular fluid in these sites does not pass through conventional lym
phatics, although proteins placed in these sites do leave them and can have
immunological efects. Privileged sites are generally surrounded by tissue
barriers that exclude naive lymphocytes. The brain, for example, is guarded
by the blood-brain barrier. Second, soluble factors, presumably cytokines,
that affect the course of an immune response are produced in privileged sites
and leave them together with antigens. The anti-inflammatory transforming
growth factor (TGF)-� seems to be particularly important in this regard.
in homeostatic conditions (that is, in the absence of infection and thus of pro
infammatory signals), antigens recognized in concert with TGF-� tend to
induce regulatory T-cell responses that do not damage tissues, rather than
pro-infammatory TH17 responses, which are induced by TGF-� in the pres
ence of IL-6 co-signaling . Third, the expression of Fas ligand
by the tissues of immunologically privileged sites may provide a futher level
of protection by inducing the apoptosis of Fas-bearing efector lymphocytes
that enter these sites.
Paradoxically, the antigens sequestered in immunologically privileged sites
are ofen the targets of autoimmune attack; for example, brain autoantigens
such as myelin basic protein are targeted in the autoimmune disease mul
tiple sclerosis, a chronic inflammatory demyelinating disease of the central
nervous system . It is therefore clear that the tolerance normally
shown to this antigen cannot be due to previous deletion of the self-reactive T
cells. In the condition experimental autoimmune encephalomyelitis (E),
a mouse model for multiple sclerosis, mice become diseased only when they
are deliberately immunized with myelin basic protein, which causes substan
tial infltration of the brain with antigen-specifcTH17 and THl cells that coop
erate to induce a local inflammatory response that damages nerve tissue.
This shows that at least some antigens expressed in immunologically privi
leged sites induce neither tolerance nor lymphocyte activation in normal cir
cumstances, but if autoreactive lymphocytes are activated elsewhere, these
autoantigens can become targets for autoimmune attack. It seems plausible
that T cells specifc for antigens sequestered in immunologically privileged
sites are most likely to be in a state of immunological ignorance. Further evi
dence comes from the eye disease sympathetic ophthalmia (Fig. 15.8). If
one eye is ruptured by a blow or other trauma, an autoimmune response to
eye proteins can occur, although this happens only rarely. Once the response
is induced, it often attacks both eyes. Immunosuppression-and, rarely,
removal of the damaged eye, the source of antigen-is required to preserve
.vision in the undamaged eye
It is not surprising that efector T cells can enter immunologically privileged
sites: such sites can become infected, and effector cells must be able to enter
these sites during infection. Effector T cells enter most or all tissues after
activation but accumulation of cells is seen only when anti
gen is recognized in the site, triggering the production of cytokines that alter
tissue barriers.
---- دو نوشته به هم متصل شده است ----
.
منبع : janeway immunology 8th ed
Tissue grafts placed in some sites in the body do not elicit immune responses.
For instance, the brain and the anterior chamber of the eye are sites in which
tissues can be grafed without inducing rejection. Such locations are termed
immunologically privileged sites (Fig. 15.7). It was originally believed that
immunological privilege arose from the failure of antigens to leave privileged
sites and induce immune responses. Subsequent studies have shown that
antigens do leave these sites and that they do interact with T cells. Instead of
eliciting a destructive immune response, however, they induce tolerance or a
response that is not destructive to the tissue.
Immunologically privileged sites are: brain - eye -testis -uterus -hamster cheek pouch
Immunologically privileged sites seem to be unusual in three ways. First, the
communication between the privileged site and the body is atypical in that
extracellular fluid in these sites does not pass through conventional lym
phatics, although proteins placed in these sites do leave them and can have
immunological efects. Privileged sites are generally surrounded by tissue
barriers that exclude naive lymphocytes. The brain, for example, is guarded
by the blood-brain barrier. Second, soluble factors, presumably cytokines,
that affect the course of an immune response are produced in privileged sites
and leave them together with antigens. The anti-inflammatory transforming
growth factor (TGF)-� seems to be particularly important in this regard.
in homeostatic conditions (that is, in the absence of infection and thus of pro
infammatory signals), antigens recognized in concert with TGF-� tend to
induce regulatory T-cell responses that do not damage tissues, rather than
pro-infammatory TH17 responses, which are induced by TGF-� in the pres
ence of IL-6 co-signaling . Third, the expression of Fas ligand
by the tissues of immunologically privileged sites may provide a futher level
of protection by inducing the apoptosis of Fas-bearing efector lymphocytes
that enter these sites.
Paradoxically, the antigens sequestered in immunologically privileged sites
are ofen the targets of autoimmune attack; for example, brain autoantigens
such as myelin basic protein are targeted in the autoimmune disease mul
tiple sclerosis, a chronic inflammatory demyelinating disease of the central
nervous system . It is therefore clear that the tolerance normally
shown to this antigen cannot be due to previous deletion of the self-reactive T
cells. In the condition experimental autoimmune encephalomyelitis (E),
a mouse model for multiple sclerosis, mice become diseased only when they
are deliberately immunized with myelin basic protein, which causes substan
tial infltration of the brain with antigen-specifcTH17 and THl cells that coop
erate to induce a local inflammatory response that damages nerve tissue.
This shows that at least some antigens expressed in immunologically privi
leged sites induce neither tolerance nor lymphocyte activation in normal cir
cumstances, but if autoreactive lymphocytes are activated elsewhere, these
autoantigens can become targets for autoimmune attack. It seems plausible
that T cells specifc for antigens sequestered in immunologically privileged
sites are most likely to be in a state of immunological ignorance. Further evi
dence comes from the eye disease sympathetic ophthalmia (Fig. 15.8). If
one eye is ruptured by a blow or other trauma, an autoimmune response to
eye proteins can occur, although this happens only rarely. Once the response
is induced, it often attacks both eyes. Immunosuppression-and, rarely,
removal of the damaged eye, the source of antigen-is required to preserve
.vision in the undamaged eye
It is not surprising that efector T cells can enter immunologically privileged
sites: such sites can become infected, and effector cells must be able to enter
these sites during infection. Effector T cells enter most or all tissues after
activation but accumulation of cells is seen only when anti
gen is recognized in the site, triggering the production of cytokines that alter
tissue barriers.
---- دو نوشته به هم متصل شده است ----
.
پاسخ : جفت
خواهش می کنم .....
Ordinarily, a woman’s body will reject a foreign organ, such as
a kidney or heart, but it will accept the fetus growing within
her womb. This acceptance exists even though half of the fetus’
genetic information has come from a “foreigner”—namely, the
father. Has her immune system failed?
Apparently not. It seems that the sperm carries an antigenic
signal that induces the woman’s immune system to produce a
series of so-called blocking antibodies. The blocking antibodies
form a type of protective screen that protects the fetus and pre-
vents its antigens from stimulating the production of rejection
antibodies by the mother. In addition, regulatory T cells (Treg),
which congregate in the womb, dampen the activity of the lym-
phocytes, helping protect the fetus from rejection.
Sometimes, however, a rejection in the form of a miscarriage
occurs. Research indicates the level of blocking antibodies and
Treg cells in some pregnant women is too low to protect the
fetus. Ironically, the low immune resistance may be because the
father’s tissue is very similar to the mother’s. In such a case, the
sperm’s antigens elicit a weak antibody and Treg response, too
low to protect the fetus. Perhaps the selection of a mate with a
similar MHC should be avoided (see MicroFocus 21.2).
Physicians are now attempting to boost the level of blocking antibodies as a way of preventing miscar-
riage. They inject white blood cells from the father into the mother, thereby stimulating her immune sys-
tem to produce antibodies to the cells. These antibodies exhibit the blocking effect.
In other experiments, injections of blocking antibodies are administered to augment the woman’s nor-
mal supply. Both approaches have been successful in trial experiments, and continuing research has given
cause for optimism that cases of fetal rejection can give way to acceptance and a full-term delivery.
تناقضی که گفتم با کتاب alcamo fundamentals of microbiology 9th ed (متن بالا) وجود دارد قسمتی است که ان را bold کرده ام . این قسمت را در کتاب های ایمونولوژی که من دیده ام وجود نداشت . اگر کسی به کتاب ایمونولوژی ابوالعباس دسترسی دارد خوهشمندم نگاه کند جواب این سوال را چه گفته است و ایا این قسمت bold را مطرح کرده است یا نه؟
بسيار عالي
با تشكر
با تشكر
Ordinarily, a woman’s body will reject a foreign organ, such as
a kidney or heart, but it will accept the fetus growing within
her womb. This acceptance exists even though half of the fetus’
genetic information has come from a “foreigner”—namely, the
father. Has her immune system failed?
Apparently not. It seems that the sperm carries an antigenic
signal that induces the woman’s immune system to produce a
series of so-called blocking antibodies. The blocking antibodies
form a type of protective screen that protects the fetus and pre-
vents its antigens from stimulating the production of rejection
antibodies by the mother. In addition, regulatory T cells (Treg),
which congregate in the womb, dampen the activity of the lym-
phocytes, helping protect the fetus from rejection.
Sometimes, however, a rejection in the form of a miscarriage
occurs. Research indicates the level of blocking antibodies and
Treg cells in some pregnant women is too low to protect the
fetus. Ironically, the low immune resistance may be because the
father’s tissue is very similar to the mother’s. In such a case, the
sperm’s antigens elicit a weak antibody and Treg response, too
low to protect the fetus. Perhaps the selection of a mate with a
similar MHC should be avoided (see MicroFocus 21.2).
Physicians are now attempting to boost the level of blocking antibodies as a way of preventing miscar-
riage. They inject white blood cells from the father into the mother, thereby stimulating her immune sys-
tem to produce antibodies to the cells. These antibodies exhibit the blocking effect.
In other experiments, injections of blocking antibodies are administered to augment the woman’s nor-
mal supply. Both approaches have been successful in trial experiments, and continuing research has given
cause for optimism that cases of fetal rejection can give way to acceptance and a full-term delivery.
پاسخ : جفت
یه چیز دیگه ای که تازه پیدا کردم و حرف کتاب بالا را تقریبا تایید می کند این است :
منبع :Sex Hormones and Immunity to Infection
By Craig. Roberts
2010
یه چیز دیگه ای که تازه پیدا کردم و حرف کتاب بالا را تقریبا تایید می کند این است :
منبع :Sex Hormones and Immunity to Infection
By Craig. Roberts
2010
....
in the placenta there is an increase presence of Asymmetric antibodies which are characterized by the presence of glycosylation on one branch of Fab region . the antibodies can still bind fetal antigen but the effector functions such as the ability to promote phagocytosis and fix complement are inactivated. therefore these Asymmetric antibodies can act as 'blocking antibodies' to mask fetal antigens.
in the placenta there is an increase presence of Asymmetric antibodies which are characterized by the presence of glycosylation on one branch of Fab region . the antibodies can still bind fetal antigen but the effector functions such as the ability to promote phagocytosis and fix complement are inactivated. therefore these Asymmetric antibodies can act as 'blocking antibodies' to mask fetal antigens.
پاسخ : جفت
چرا راه دور مي ريد...
٣ تا فرضيه وجود داره :
يك ) تروفوبلاست با ترشح hcg و يه سري PG و اينترلوكين و ... باعث كاهش اثر لنفوسيت هاي T مادر ميشه
دو) تروفوبلاست يك هورمون ترشح مي كنه كه باعث آپوپتوز لنفوسيت هاي تي مي شه
سه) تروفوبلاست با ترشح يه ماده ، يه آمينو اسيد (يادم نيست كودوم آمينواسيد) مورد نياز لنفوسيت هاي تي رو از بين مي بره
با اين حالات چون فقط لنفوسيت هاي خاصي كه به آنتي ژن هاي جفت حساسيت دارند از بين مي رن و بقيه سيستم ايمني مشكلي خاصي پيدا نمي كنه (البته فرض سه كلي هست)
والا من اين رو از كمپبل يادم مياد ...
چرا راه دور مي ريد...
٣ تا فرضيه وجود داره :
يك ) تروفوبلاست با ترشح hcg و يه سري PG و اينترلوكين و ... باعث كاهش اثر لنفوسيت هاي T مادر ميشه
دو) تروفوبلاست يك هورمون ترشح مي كنه كه باعث آپوپتوز لنفوسيت هاي تي مي شه
سه) تروفوبلاست با ترشح يه ماده ، يه آمينو اسيد (يادم نيست كودوم آمينواسيد) مورد نياز لنفوسيت هاي تي رو از بين مي بره
با اين حالات چون فقط لنفوسيت هاي خاصي كه به آنتي ژن هاي جفت حساسيت دارند از بين مي رن و بقيه سيستم ايمني مشكلي خاصي پيدا نمي كنه (البته فرض سه كلي هست)
والا من اين رو از كمپبل يادم مياد ...