FOXP3 Promoter Demethylation Reveals the Committed Treg Population in Humans

Background: A report last year suggests that loss of regulatory T cells may contribute to chemical sensitivity from environmental exposures. As this author describes, "the transcription factor FOXP3 is crucial for the suppressive activity of Tregs and is considered the most specific marker for this population.....The results of his most recent findings show that "only complete demethylation of the conserved FOXP3 promoter region support stable long term FOXP3 expression and a committed Treg phenotype in humans."

CiteULike: FOXP3 Promoter Demethylation Reveals the Committed Treg Population in Humans: "Janson, P. C. J., Winerdal, M. E., Marits, P., Thörn, M., Ohlsson, R., and Winqvist, O. (2008). Foxp3 promoter demethylation reveals the committed treg population in humans. PLoS ONE, 3(2):e1612+."
Mićović, V., Vojniković, B., Bulog, A., Coklo, M., Malatestinić, D., and Mrakovcić-Sutić, I. (2009). Regulatory t cells (tregs) monitoring in environmental diseases. Collegium antropologicum, 33(3):743-746.http://www.citeulike.org/group/6057/article/6090770

Myelin Basic Protein Priming Reduces the Expression of Foxp3 in T Cells via Nitric Oxide.

In a preceding blog, we discussed how FOXP3 in important for autoimmune suppressing T cells. We also described how a recent study suggests that the loss of Tregs may be a contributing factor in chemical sensitivity and environmental illnesses from exposures to air contaminants. Here we see that NO is a factor in the altered expression in FOX3P Tregs.


CiteULike: Myelin Basic Protein Priming Reduces the Expression of Foxp3 in T Cells via Nitric Oxide.: "Brahmachari, S. and Pahan, K. (2010). Myelin basic protein priming reduces the expression of foxp3 in t cells via nitric oxide. Journal of immunology (Baltimore, Md. : 1950)."

Commensal Bacteria Induce Tolerance via Tregs and Anti-Inflammatory Cytokine in Gut~!

Background: It has been suggested that multiple chemical sensitivity may be a consequence of loss of tolerance and (Tregs) by the immune system. In addition, this condition may also influence other environmental illnesses as well. One would assume any environmental condition that disturbs the natural environment of the intestinal tract could lead to the potential for chemical sensitivity if this is true. Considering this to be true, anything that improves healthy gut flora and reduces inflammation may be of benefit to those who suffer from this condition.

"Bacteroides fragilis, directs the development of Foxp3(+) regulatory T cells (Tregs) with a unique 'inducible' genetic signature. Monocolonization of germ-free animals with B. fragilis increases the suppressive capacity of Tregs and induces anti-inflammatory cytokine production exclusively from Foxp3(+) T cells in the gut. We show that the immunomodulatory molecule, polysaccharide A (PSA), of B. fragilis mediates the conversion of CD4(+) T cells into Foxp3(+) Treg cells that produce IL-10 during commensal colonization. Functional Foxp3(+) Treg cells are also produced by PSA during intestinal inflammation, and Toll-like receptor 2 signaling is required for both Treg induction and IL-10 expression"

Inducible Foxp3+ regulatory T-cell development by ... [Proc Natl Acad Sci U S A. 2010] - PubMed result:

View Similar Posts: Tregs

Activation of the aryl hydrocarbon receptor induces human type 1 regulatory T cell-like and Foxp3(+) regulatory T cells.

"induction of functional Foxp3(+) iT(reg) cells required coordinated action of the transcriptional regulators Smad1 and Aiolos. Thus, AhR is a potential target through which functional iT(reg) cells could be induced in human autoimmune disorders."

Read more: CiteULike: Activation of the aryl hydrocarbon receptor induces human type 1 regulatory T cell-like and Foxp3(+) regulatory T cells.

:"Gandhi, R., Kumar, D., Burns, E. J., Nadeau, M., Dake, B., Laroni, A., Kozoriz, D., Weiner, H. L., and Quintana, F. J. (2010). Activation of the aryl hydrocarbon receptor induces human type 1 regulatory t cell-like and foxp3(+) regulatory t cells. Nature immunology."

T Regulatory Cells in Cord Blood-FOXP3 Demethylati... [PLoS One. 2010] - PubMed result

T Regulatory Cells in Cord Blood-FOXP3 Demethylati... [PLoS One. 2010] - PubMed result: "T Regulatory Cells in Cord Blood-FOXP3 Demethylation as Reliable Quantitative Marker."

Allergen exposure increases Th2-cytokines and FOXP3 expression in asthmatic lungs

MedWire News - Respiratory - Allergen exposure increases Th2-cytokines and FOXP3 expression in asthmatic lungs: "Allergen exposure increases Th2-cytokines and FOXP3 expression in asthmatic lungs"

FOXP3(+) CD4(+) Tregs lose suppressive potential but remain anergic during transient inflammation in human.

A loss of the suppressive function of Tregs have been implicated as a possible contributor to chemical sensitivity. This new study suggests that inflammation can cause a loss of Tregs suppressive function. This suggests that periods where inflammation is higher may contribute to chemical sensitivity.

Read Abstract: CiteULike: FOXP3(+) CD4(+) Tregs lose suppressive potential but remain anergic during transient inflammation in human.: "European journal of immunology (9 February 2011) doi:10.1002/eji.201040363 Key: citeulike:8982549"

Antigen-Specific CD25-Foxp3-IFN-{gamma}highCD4+ T Cells Restrain the Development of Experimental Allergic Encephalomyelitis by Suppressing Th17.

Antigen-Specific CD25-Foxp3-IFN-{gamma}highCD4+ T Cells Restrain the Development of Experimental Allergic Encephalomyelitis by Suppressing Th17.

[Effect of cigarette smoke on Tregs and Foxp3 in Asthma~!

Wow---How did I miss this?


[Effect of cigarette smoke exposure on the percent... [Zhonghua Jie He He Hu Xi Za Zhi. 2010] - PubMed result: "[Effect of cigarette smoke exposure on the percentage of CD(4)(+)CD(25)(+) regulatory T cells and the expression of transcription factor Foxp3 in asthmatic rats.]"

Antigen-Specific CD25-Foxp3-IFN-{gamma}highCD4+ T Cells Restrain the Development of Experimental Allergic Encephalomyelitis by Suppressing Th17.

Antigen-Specific CD25-Foxp3-IFN-{gamma}highCD4+ T Cells Restrain the Development of Experimental Allergic Encephalomyelitis by Suppressing Th17.

Light Therapy Decreases Certain Immune Complexes While Increasing Tregs in psoriasis-like condition~!

PUVA induced the Th2 pathway and IL-10-producing CD4+CD25+Foxp3+Tregs with disease-suppressive activity that was abolished by anti-CTLA4 mAb treatment. These findings were paralleled by macroscopic and microscopic clearance of the diseased murine skin. Anti-IL-17 mAb treatment also diminished the psoriatic phenotype of the mice. This indicated that both induced Tregs involving CTLA4 signaling and inhibition of the IL-23/Th17 axis are central for the therapeutic action of PUVA.

CiteULike: 8-methoxypsoralen plus ultraviolet A therapy acts via inhibition of the IL-23/Th17 axis and induction of Foxp3+ regulatory T cells involving CTLA4 signaling in a psoriasis-like skin disorder.: "Singh, T. P. P., Schön, M. P., Wallbrecht, K., Michaelis, K., Rinner, B., Mayer, G., Schmidbauer, U., Strohmaier, H., Wang, X.-J. J., and Wolf, P. (2010). 8-methoxypsoralen plus ultraviolet a therapy acts via inhibition of the il-23/th17 axis and induction of foxp3+ regulatory t cells involving ctla4 signaling in a psoriasis-like skin disorder. Journal of immunology (Baltimore, Md. : 1950), 184(12):7257-7267."

Vitamin D may treat and prevent allergic reaction to mold in cystic fibrosis patients

Comment: The following study helps support the HEIRS and others' hypothesis that MCS and other environmental illnesses are a "loss of tolerance" which involves impaired Treg production.


"PITTSBURGH, Aug. 25 – Vitamin D may be an effective therapy to treat and even prevent allergy to a common mold that can cause severe complications for patients with cystic fibrosis and asthma, according to researchers from Children's Hospital of Pittsburgh of UPMC, the University of Pittsburgh School of Medicine and Louisiana State University School of Medicine."

Read more: Vitamin D may treat and prevent allergic reaction to mold in cystic fibrosis patients:

For further reading: Tregs, loss of tolerance, FoxP3
     **********You can also search the HEIRS Citation database for related citations.


Duan, W., So, T., and Croft, M. (2008). Antagonism of airway tolerance by endotoxin/lipopolysaccharide through promoting ox40l and suppressing antigen-specific foxp3+ t regulatory cells. Journal of immunology (Baltimore, Md. : 1950), 181(12):8650-8659.   http://www.citeulike.org/user/HEIRS/article/3752381

Ammonia Enzymes, Immune Cells & X-Linked Mutations In Autoimmunity and Disease

Background: We have suggested that environmental illnesses may involve the loss of suppression of regulatory T cells and that several different proteins may be involved which changes the dynamics or "immunological footprint" of these conditions in each individual. Previously we mentioned how high ammonia levels may account for some of the symptoms associated with multiple chemical sensitivity. We also noted recently how alterations in ornithine enzymes may effect ammonia levels and the Nrf2 gene regulator has some control over its expression. The following article discusses findings related to how a mutation in ornithine transcarbamalase may influence the immune system and play a role in autoimmune type disease. Interestingly, the author points out the condition is X-linked which might account for higher number of females presenting with them because males usually die in utero and do not live but a few days after birth. There is usually a large sexual dimorphism in the prevalence of many environmental diseases. As Li explains, there may be a number of factors that contribute to autoimmune disease which may include estrogenic production as well as, vulnerable phenotypes may be more susceptible to metals exposure which may accelerate some individuals to reactive phenotypes. (Li)

The author writes, "Antigen expression in the thymus leads to the deletion of self-reactive T cells and generation of regulatory lymphocytes, including regulatory T cells(Treg) and NKT cells. We show an Ornithine transcarbamylase(OTC) mutation causes ineffective presentation of self antigens in the thymus. As such, deletion of self reactive T cells is compromised and production of Treg and NKT cells is reduced in the OTC mutant mice. More importantly the heterozygous mice have increased susceptibility to autoimmune diseases, including the generation of autoantibodies and more severe EAE." Further, "OTC mutant mice, the production of Treg in the thymus is reduced, which is correlated with the impaired antigen presentation due to hyperammonemia."


Comment: This article is a good representation of why only qualified medical professionals that understand the multitude of genetic conditions and environmental conditions that activate them should be treating them. There is no evidence thus far, that a "therapeutic recipe" is effective at treating all of them.


Chang, X. (2006). X linked foxp3 & otc in immune tolerance and autoimmunity. Ohio State University. http://www.citeulike.org/user/HEIRS/article/6650098
Li, J., Stein, T. D., and Johnson, J. A. (2004). Genetic dissection of systemic autoimmune disease in nrf2 deficient mice. Physiological Genomics.
http://www.citeulike.org/user/HEIRS/article/6604948

Regulatory T Cell (Tregs) Production Dependant on Methylation Modifications~!

Background: New report support that the balance of Tregs need to be maintained for suppression of immune functions that lead to autoimmune-type reactions including those that may be seen in diabetes, colitis and lupus. In previous blogs, I suggest that loss of Tregs may influence the development of chemical sensitivity through the loss of Treg suppression and "loss of tolerance" and has been suggested by other authors. In the past, I have also reviewed several research studies that identify how recent findings of aberrant methylation influence environmental disease including autism, endometriosis and PTSD.

Interesting the following study by Floess shows that epigenetic modifications must occur with immune cells for cells to develop into "suppressor-type" lineages of Tregs. Therefore, alterations in methylation may negatively influence the development of Treg cells and could cause or augment environmental disease. This also provides a mechanism for what appears an inheritability of environmental disease.

Floess, S., Freyer, J., Siewert, C., Baron, U., Olek, S., Polansky, J., Schlawe, K., Chang, H.-D., Bopp, T., Schmitt, E., Klein-Hessling, S., Serfling, E., Hamann, A., and Huehn, J. (2007). Epigenetic control of the foxp3 locus in regulatory t cells. PLoS Biol, 5(2):e38+.
http://www.citeulike.org/user/HEIRS/article/1080288

Elevating Tregs and Heat Shock Proteins in EI - The Role of Food and Exercise

Background: In a recent blog, we expressed an interest in a recent study that showed alterations in the distributions of suppressive T cells called Tregs which may influence environmental illness.(Micovic) According to the author, these cells are normally upregulated upon chronic inhalation of pollutants but in this case, the researcher noted a decrease in these suppressive cells. In other studies, a decrease in Foxp3 Tregs are often associated with autoimmune-like conditions. In addition, we also discussed a study the showed that particulate matter may alter "immunological footprints" and may lead to a autoimmune-like presentation. Also, regulatory Treg suppression plays a role in protection of striatal neurons and reductions of microglial neuroinflammation and alpha-synuclein and therefore, Tregs may play an important protective role in Parkinson's disease. It also suggests an explanation of how environmental exposures may contribute to PD and other neurodegenerative diseases. Catecholamines have been shown to downregulate the expression of Tregs and this is dependant on the expression of the dopamine D1-like receptors.

Other studies have revealed some insights into the relationship of Tregs and other proteing called heat shock proteins. Heat shock proteins are normally considered protective and often chaperone proteins during specific metabolic processes. De Zoeten recently showed that Tregs with HSP70 had more suppressive effects than those without. It was concluded that at least for this study of colitis, there was an important interaction with HSP70 and FoxP3+. Interestingly, a recent CFS study which is often co-morbid with colitis, demonstrated altered profiles of a number of heat shock proteins including HSP70 (Jammes) and suggested these proteins may be used as a biomarker for CFS. Wieten describes heat shock proteins as proteins that are normally upregulated in response to stress, including thermal and oxidative stress and inflammation and help prevent cellular damage by increasing the expression of anti-inflammatory T cells.

Weiten explains that by elevating the levels of heat shock proteins, an individual may be able to restore or increase their resistance to cellular stress. Weiten provides evidence that dietary phytonutrients can elevate levels of heat shock proteins. In his study, he found that several compounds found in food elevated HSP70 that elevated the expression of T cells. One such compound called carvacol is found in thyme and oregano. In other blogs, we have noted that the latter is associated with expression of PPAR-gamma which has anti-inflammatory properties. Hontecillas demonstrates in his research that PPAR-gamma can influence the activity of Tregs against inflammation. This seems to entail down-regulation of certain other T cells (Konturek) and as we have noted numerous times before, PPAR-gamma expression can be influenced by the expression of Nrf2.

Different studies have shown positive and negative consequences of exercise on environmental illnesses and this may be dependant on the levels of expression of a number of different proteins. In any case, it has been demonstrated that exercise positively influences the expression of HSP70.(Milne)Researchers from University of Alabama at Birmingham recently demonstrated that Treg cells in exercised mice increased cells with FoxP3+ and were better able to fascilitate suppression of inflammatory cytokines in an experimental model of murine asthama. In contrast, increasing age may negatively influence the expression of both Tregs and HSP70. Also, exposure to paraquat decreases expression of both HO-1 and HSP70 and increases oxidation of proteins. (Nakanishi) Muscle atrophy is often associated with aging and serious illness; the prevention of which can be influenced by the expression of HSP70. (Senf) Other studies show HSP are regulated through exercise-induced SIRT1 but interactions with HSP regulation is not the only way SIRT1 is involved in immune regulation. Reports now show that the dysregulation of SIRT1 leads to abnormal T cells responses and loss of tolerance and the development of autoimmunity. Zhang explains that while SIRT1 regulation is required for normal T cell activity, this responsibility does not involve maintaining Treg function or Th17 but does involve control of autoreactive T cells. In contrast, van Loosdregt mentions that use of HDAC inhibitors may be an alternative method for modulating FoxP3+ in Tregs. So it seems, the level of involvement of SIRT1 of Treg function is not at all clear and needs further study. In any case, the findings of the studies above, definitively demonstrate the importance of both Nrf2 and SIRT1 in regulation/dysregulation of immune function in a number of environmental illnesses.


Mićović, V., Vojniković, B., Bulog, A., Coklo, M., Malatestinić, D., and Mrakovcić-Sutić, I. (2009). Regulatory t cells (tregs) monitoring in environmental diseases. Collegium antropologicum, 33(3):743-746. http://www.citeulike.org/user/HEIRS/article/6090770
De Zoeten, E. F., Wang, L., Sai, H., Dillmann, W. H., and Hancock, W. W. (2009). Expression of hdac9 by t regulatory cells prevents colitis in mice. Gastroenterology. http://www.citeulike.org/user/HEIRS/article/6553713
Wieten, L., van der Zee, R., Goedemans, R., Sijtsma, J., Serafini, M., Lubsen, N. H., van Eden, W., and Broere, F. (2010). Hsp70 expression and induction as a readout for detection of immune modulatory components in food. Cell stress & chaperones, 15(1):25-37.
http://www.citeulike.org/user/HEIRS/article/4675555
Senf, S. M., Dodd, S. L., and Judge, A. R. (2010). Foxo signaling is required for disuse muscle atrophy and is directly regulated by hsp70. American journal of physiology. Cell physiology, 298(1).
http://www.citeulike.org/user/HEIRS/article/6553728
Nakanishi, Y. and Yasumoto, K. (1997). Induction after administering paraquat of heme oxygenase-1 and heat shock protein 70 in the liver of senescence-accelerated mice. Bioscience, biotechnology, and biochemistry, 61(8):1302-1306.
http://www.citeulike.org/group/7833/article/6553731
Konturek, P. C., Dembinski, A., Warzecha, Z., Burnat, G., Ceranowicz, P., Hahn, E. G., Dembinski, M., Tomaszewska, R., and Konturek, S. J. (2005). Pioglitazone, a specific ligand of peroxisome proliferator-activated receptor-gamma, protects pancreas against acute cerulein-induced pancreatitis. World journal of gastroenterology : WJG, 11(40):6322-6329.
http://www.citeulike.org/user/HEIRS/article/6553866
Hontecillas, R. and Bassaganya-Riera, J. (2007). Peroxisome proliferator-activated receptor gamma is required for regulatory cd4+ t cell-mediated protection against colitis. Journal of immunology (Baltimore, Md. : 1950), 178(5):2940-2949.
Milne, K. J. and Noble, E. G. (2002). Exercise-induced elevation of hsp70 is intensity dependent. Journal of applied physiology (Bethesda, Md. : 1985), 93(2):561-568.
http://www.citeulike.org/user/HEIRS/article/6553732
Senf, S. M., Dodd, S. L., and Judge, A. R. (2010). Foxo signaling is required for disuse muscle atrophy and is directly regulated by hsp70. American journal of physiology. Cell physiology, 298(1). http://www.citeulike.org/user/HEIRS/article/6553728
Lowder, T., Dugger, K., Deshane, J., Estell, K., and Schwiebert, L. M. (2010). Repeated bouts of aerobic exercise enhance regulatory t cell responses in a murine asthma model. Brain, behavior, and immunity, 24(1):153-159. http://www.citeulike.org/user/HEIRS/article/5842541
Reynolds, A. D., Banerjee, R., Liu, J., Gendelman, H. E., and Mosley, R. L. (2007). Neuroprotective activities of cd4+cd25+ regulatory t cells in an animal model of parkinson's disease. Journal of leukocyte biology, 82(5):1083-1094. http://www.citeulike.org/user/HEIRS/article/6554146
Cosentino, M., Fietta, A. M., Ferrari, M., Rasini, E., Bombelli, R., Carcano, E., Saporiti, F., Meloni, F., Marino, F., and Lecchini, S. (2007). Human cd4+cd25+ regulatory t cells selectively express tyrosine hydroxylase and contain endogenous catecholamines subserving an autocrine/paracrine inhibitory functional loop. Blood, 109(2):632-642. http://www.citeulike.org/user/HEIRS/article/6554165
Iwata, S., Shimizu, T., Nomoto, M., and Fukuda, T. (1996). Characteristic upregulation of dopamine d1-receptor in rat striatum after 6-hydroxydopamine treatment. Japanese journal of pharmacology, 71(3):255-258.
http://www.citeulike.org/user/HEIRS/article/6554215
It is Hot in Here, or is it Just SIRT1. SIRT1 Activate Heat Shock Transcription. Retrieved on January 16, 2010.
Zhang, J., Lee, S.-M. M., Shannon, S., Gao, B., Chen, W., Chen, A., Divekar, R., McBurney, M. W., Braley-Mullen, H., Zaghouani, H., and Fang, D. (2009). The type iii histone deacetylase sirt1 is essential for maintenance of t cell tolerance in mice. The Journal of clinical investigation, 119(10):3048-3058.
http://www.citeulike.org/user/HEIRS/article/6554270
Jammes, Y., Steinberg, J. G., Delliaux, S., and Brégeon, F. (2009). Chronic fatigue syndrome combines increased exercise-induced oxidative stress and reduced cytokine and hsp responses. Journal of internal medicine, 266(2):196-206. http://www.citeulike.org/user/HEIRS/article/4695048

Chemical Sensivity and Asthma -- Systems Theory and The Idea of Loss of Tolerance in Different Tissues!

In the last few years, environmental illness researchers have suggested that chemical sensitivity is related to a general loss of tolerance that may occur after an event such as bacterial or viral event. Of course, this would make sense given that an inflammatory event may lead to loss of tolerance through alterations in immune function and some experts believe a similar process is responsible for autoimmune-type reactions and a loss of T regulatory cells (Tregs). In general, Treg serve as a type of mediator for inflammatory conditions and modulates the type and severity of the immune reaction. In MCS, there is a loss of tolerance to chemicals in the environment at levels that normally do not effect a healthy individual. Interestingly, a recent study of asthma has shown that hypersensitivity airway responsiveness can be improved by boosting immunity in the gut. The fact that airway responsiveness can be improved through gut improvement helps to support the possibility that MCS immune dysfunction may begin in the intestinal tract or the lungs even though symptoms may not necessarily be respiratory or gut related. It has been known for two decades, the intestinal tract is an important regulator of immune and brain function but admittedly, little is known about the pathways or the process involved that makes the connections of the intestinal tract, the brain and the CNS. However, studies published last year identified inflammatory brain processes that effect gene regulation and neurotransmission can be the result of the activities of inflammatory mediators or cytokines in the gut and the liver.

Individuals with MCS often present with abnormal respiratory function and many that suffer from MCS propose they are more sensitive to carbon monoxide and hydrogen sulfide than others. I would suggest through observation this is also true of nitrous oxide and possibly other greenhouse gases and note here there have been reports of mood and behavior changes from exposures to higher levels of these gases. These reports are similar to many with MCS when they describe their reported reactive symptoms. Therefore these reactions could be the result from elevations in greenhouse gases in addition to other pollutants that combine to form explained additional "triggers".   Previously, I have suggested the loss of Nrf2 and its associated proteins such as HO-1 that regulate the gasotransmitters may be to blame and could lead to loss of tolerance or heightened reaction even to lower levels of "perceived" pollutants or chemicals in the environment.  Considering the levels of greenhouse gases are steadily increasing on the average in the environment with each decade-- the constant exposure to one may be reducing the tolerance to the cumulative total of the others or "potentiating" the effects. This brings to light an important health and policy concern since the "jury" is still out on how to reduce greenhouse gases with our present dependance on fossil fuels. Interestingly, you never really hear about the increases in greenhouse gases in relation to the causes and implications of MCS, even though it should be considered...

In any case, there is recent evidence the proteins that make up the xenobiotic detoxification system such as the Nrf2, AhR, and HO-1 may influence Treg regulation. For this reason, the effects of Treg deficiency and dysfunction should be considered why addressing the possible causes for increased sensitivities that are observed in those effected with environmental illness and why boosting gut immunity of systemic immunity may influence more than one organ system. In addition, it has been demonstrated that endotoxin a component of bacteria may lead to a heightened response from allergans. It could be endotoxic exposure leads to a heightened response to chemicals or contaminants whether endogenous or not and alterations in methylation from endotoxin may augment conditions of the "loss of tolerance" that that lead to and occur with environmental illness. Unfortunately, this "loss of tolerance" may also be the consequence of pathogens and contaminants that normally reside at low levels in different tissue and are present in the environment.




Strickland, D. H., Judd, S., Thomas, J. A., Larcombe, A. N., Sly, P. D., and Holt, P. G. (2010). Boosting airway t-regulatory cells by gastrointestinal stimulation as a strategy for asthma control. Mucosal immunology. http://www.citeulike.org/user/HEIRS/article/7560150
Chapman, J. T., Otterbein, L. E., Elias, J. A., and Choi, A. M. K. (2001). Carbon monoxide attenuates aeroallergen-induced inflammation in mice. Am J Physiol Lung Cell Mol Physiol, 281(1):L209-216. http://www.citeulike.org/user/HEIRS/article/7560177
Zhou, X., Kong, N., Zou, H., Brand, D., Li, X., Liu, Z., and Zheng, S. G. G. (2010). Therapeutic potential of tgf-beta-induced cd4(+) foxp3(+) regulatory t cells in autoimmune diseases. Autoimmunity. http://www.citeulike.org/user/HEIRS/article/7560254
Fousteri, G., Dave, A., Bot, A., Juntti, T., Omid, S., and von Herrath, M. (2010). Subcutaneous insulin b:9-23/ifa immunisation induces tregs that control late-stage prediabetes in nod mice through il-10 and ifngamma. Diabetologia, 53(9):1958-1970. http://www.citeulike.org/user/HEIRS/article/7299083