Are gamma delta T cells involved in T cell activation?
146453
Although gamma delta T cell receptor-bearing lymphocytes (gamma delta T cells) constitute a significant minority of circulating and tissue-associated T lymphocytes, the mechanism responsible for the activation of these cells is unknown. To address this question, resting gamma delta TCR+, CD3+, CD4-, CD8- cells isolated from the blood of healthy volunteers were cultured with allogeneic dendritic cells (DC) or monocytes, and their proliferative response measured. DC alone induced gamma delta T cells to proliferate, with a peak response on the sixth day of culture. Pretreatment of DC with an anti-HLA-DR mAb, but not anti-HLA class I or anti-CD1 mAbs, inhibited the response of gamma delta T cells. Antibodies to gamma delta T cell receptor, CD2, CD3, or CD11a were also inhibitory, whereas antibodies to alpha beta T cell receptor, CD4, CD5, and CD8 had no effect. Although only 40-60% of freshly isolated gamma delta T cells expressed CD28, mAbs directed against CD28 or its ligand, CD80, were markedly inhibitory. Moreover, removal of CD28+ cells from the gamma delta T cell population nearly abrogated the response to DC. These results demonstrate that resting gamma delta T cells recognize and respond to MHC class II determinants on allogeneic DC in a manner that is highly dependent on the CD28 activation pathway as well as molecules such as CD2 and CD11a that mediate cell-to-cell adhesion.
386583
I know there are some proteins produced by prokaryotes and eukaryotes that lack a typical leader peptide sequence; for example lacking a hydrophobic leader peptide. Some of these proteins are exported to the membrane by a substrate specific ATP-driven membrane translocater. Used to be called ABC-transporters because they could bind and hydrolize ATP. I think T-cell presentation is associated with a system like this where ABC-transporters transport endogenous antigenic peptides to the ER where\nthey bind to the MHC: peptide receptor complex before being\ntransported to the cell surface. I know S. cerevisiae, MATa haploid cells, release a 12-residue posttranslationally modified lipopeptide that binds via a farnesyl\nmoiety attached via a thioether linkage to the C-terminal residue. So, basically I would suggest looking at a possible ABC-transporter or a lipopeptide. There might be other options but they escape me at the moment.
474647
Cytotoxic  or killer T cells (CD8+) do their work by releasing lymphotoxins, which cause cell lysis. Helper T cells (CD4+) serve as managers, directing the immune response. They secrete chemicals called lymphokines that stimulate cytotoxic T cells and B cells to grow and divide, attract neutrophils, and enhance the ability of macrophages to engulf and destroy microbes. Suppressor T cells  inhibit the production of cytotoxic T cells once they are unneeded, lest they cause more damage than necessary. Memory T cells  are programmed to recognize and respond to a pathogen once it has invaded and been repelled.
594197
The maternal and fetal circulatory systems only come in contact at one place--the placenta.  The mother's antigen-presenting cells can't cross the placenta, so if an immune response was going to be mounted it would be there.  Two basic ideas as to why this doesn't happen:\n\n(1) The trophoblasts that form the fetal half of the placenta don't express the usual major histocompatibility complexes that would ordinarily prompt immunological responses in adult tissues (for example, in transplant grafts).  In other words, the fetal half of the placenta is invisible to the mother's T-cells.\n\n(2) The trophoblasts that form the fetal half of the placenta produce cell surface proteins that actively suppress the mother's immune response in the vicinity of the placenta.\n\nFor a very recent (published March 2006), in-depth review, see my source....
684888
Clincial studies show thymic protein A is quite effective...you can see the studies here  http://newenglandnutritives.com/pro_boost_thymic.htm
342771
This is false. \nWhite blood cells, also known as leukocytes, are the body's defensive cells and are part of the immune system. There are different types of leukocytes, including B lymphocytes and T lymphocytes.\nB lymphocytes msture in the Bursa of Fabricius. {hence their name}\nand also include two types:\n      a) Memory B cell- these cells "remember" how to make a certain antibody in response to a particular pathogen (antigen).\n      b) Plasma B cell- secrete antibodies in order to destroy antigens. antibodies bind the antigens together to make the easier targets for the phagocytes (which "eat" them up.)\n\nT lymphocytes mature in the thymus {that's what the T stands for}. There are three kinds of T cells:\n     a)Cytotoxic T cells destroy infected cells. \n     b) Helper T cells, when activated, they proliferate and secrete cytokines that regulate or "help" effector lymphocyte function. \n     c) Regulatory T cells, also known as suppressor T cells, suppress activation of the immune system and maintain immune system homeostasis. If these fail, you get an autoimmune disease (where the immune system attacks itself!)\n\n\nOn the other hand, Red blood cells, also known as eythrocytes, carry oxygen. They have hemoglobin, which is a globular protein containing four subunit proteins found in the blood of vertebrates (organisms with a backbone). The heme group has iron in it, and this is where the oxygen binds to. This also gives blood its red color.\nRBCS are circulated by the blood.\ntheir biconcave shape (like they have a dent on both sides...) let them carry oxygen more efficiently as well. \nA disease of this, called sickle cell anemia, is when RBCs are sickle shaped and do not carry oxygen efficiently, resulting in a tired person. \nyeah.\nhave a nice day!
365428
Depends if you are doing flow cytometry testing, serology testing or DNA/PCR typing.  If you are doing serolgy testing, then usually you have pre-loaded serum panels on microplates that will be indicative of certain antigens.  You add the patients lymphocytes and incubate.  You then stain using a live dead stain, with fluorescent green indicating live cells (no cross reactivity) or red, indicating dead cells or a rejection reaction.  From these results you can decide which antige3ns the patient would potentially react (or not) with. That's the short answer as there are other lab protocols that encompass HLA testing.
524726
If the % lymphocytes was low, was anything/everything else high?  Things that can cause lymphopenia: medication side effect (is he on corticosteroids?), extensive radiation exposure, myelogenous leukemia, HIV, kidney failure (I wasn't aware of this one--but my source indicates it).  I don't think mononucleosis typically causes lymphopenia.  I think it's actually the opposite--it usually causes an increase in your % lymphocytes.
899422
Measurement of cell proliferation and cell mediated contraction in 3-dimensional hydrated collagen matrices \n\nSummary  This report describes simplified methods for the preparation of reconstituted collagen gels containing a uniform distribution of anchorage dependent cells in 96-well microtitration plates, their dissolution with collagenase allow harvesting of either cells or medium, and objective analytical methods for measuring cell mediated contraction of collagen gels and [3 H]thymidine incorporation rates.\nKey words  collagen - cell proliferation assay - contraction assay - micro cell-culture methods\n\nTo whom requests for reprints should be addressed at Opthalmic Research Unit, University of Western Australia, Royal Perth Hospital, GPO Box X2213, PERTh 6001, Western Australia.\n\n:>peace
511334
The change in morphology and behaviour of lymphocytes exposed to a mitogen or to an antigen to which they have been primed. The result is the production of lymphoblasts, cells that are actively engaged in protein synthesis and that divide to form effector populations. Should not be confused with transformation of the type associated with oncogenic viruses, and "activation" is therefore perhaps a better term.
403858
It's pretty well established that the apoptotic machinery gets deprogrammed by cells progessing through tumorogenesis.  One way is the well understood p53/Mdm2 pathway.  P53 is a tumor supressor and, upon DNA damage, can either halt cells to repair the damage (at the G1/S checkpoint) or trigger apoptosis.  It does this by promoting gene expression.  \n\nAnother mechanism is to inhibit t-cell induced apoptosis, by deregulation of FasL and other proteins.\n\nThere's a whole bunch of info in the Cancer Medicine book online at NCBI (below).
1135438
I don't think so. We don't really know what causes lymphocytic collitis - it could be autoimmune or due to a virus, so I can't really say for certain, but it's doubtful.
474181
The structural interaction between the human T-cell receptor (TCR), and the antigenic peptide as linked to a major histocompatibility complex (MHC) molecule are fundamental to the workings of the immune system. Previous work has shown that when a virus or bacteria invades the body, the immune system first breaks up cells infected by the invaders. These infected cells are 'flagged" with a combination of the foreign protein and an MHC molecule and bound to a TCR. Roving T-cells then recognize and destroy these flagged cells. \n\nBut until now, no one has known what the atomic structure of this immune interaction looked like. Harvard researchers, led by Don C. Wiley of the Department of Molecular and Cellular Biology, determined that TCR structure resembles that of another key component of the immune system, antibodies, particularly, the anitgen-binding region. This discovery led the way to the identification of the entire structure of the MHC-TCR complex. \n\nThe research indicates that the antigenic peptide produced by degradation of the invading virus within the cell is held within the MHC binding cleft almost like a hot-dog is held in a bun. This peptide and most of the MHC molecule are engulfed by the TCR. \n\nIn a related study, researchers at the University of Maryland Biotechnology Institute gained new insight into the phenomenon of superantigen creation. In some cases, the TCR-MHC interaction leads to an overreaction by T-cells. This overactive immune creates superantigens have that have been implicated in diseases and complications as varied as toxic shock syndrome, diabetes mellitus and multiple sclerosis. \n\nThe researchers showed for the first time how a superantigen protein (in this case, the peptide toxin produced by the bacterium Staphylococcus aureus) binds to the TCR. The work showed that by bringing the MHC and TCR together directly, regardless of the peptide bound to the MHC, the superantigen circumvents the normal mechanism for T-cell activation by specific peptide-MHC complexes, and triggers a more general reaction instead. \n\nThe basis for the current work can be traced back to 1974, when Drs. Rolf Zinkernagel and Peter Doherty determined that killer T-cells sense infected target cells by the identification of viral antigens displayed on the cell surface in combination with MHC proteins. This process has become known as MHC restriction. The two scientists shared the Nobel prize this year for this work.
1135871
They work through signal transduction.
1132433
Tonsils are lymph glands which are a part of your immune system.  When there is an infection, your immune system is mobilized.  And part of the response is activation and enlargement of you lymph glands including your tonsils.  The thing to remember is that only the lymph nodes around the infection will enlarge.
335689
A few sites on immunology here
557310
All the cellular components of the blood derive from the bone marrow. Erythroid progenitors give rise to red cells, megakaryocytes split themselves into tiny pieces to give platelets, and hematopoyetic pluripotent stem cell progenitors give rise to myeloid and lymphoid progenitors The first of them give rise to granulocytes (mastocytes, eosinophyls, basophyls and neutrophyls) and monocytes (which later become macrophages). The lymphoid progenitors give rise to T and B lymphocytes.