201 research outputs found
Cytomolecular identification of individual wheat-wheat chromosome arm associations in wheat-rye hybrids
Chromosome pairing in the meiotic metaphase I of wheatrye
hybrids has been characterized by sequential genomic
and fluorescent in situ hybridization allowing not only the
discrimination of wheat and rye chromosomes, but also the
identification of the individual wheat and rye chromosome
arms involved in the chromosome associations. The majority
of associations (93.8%) were observed between the wheat
chromosomes. The largest number of wheat-wheat chromosome
associations (53%) was detected between the A and D
genomes, while the frequency of B-D and A-B associations
was significantly lower (32 and 8%, respectively). Among the
A-D chromosome associations, pairing between the 3AL and
3DL arms was observed with the highest frequency, while
the most frequent of all the chromosome associations (0.113/
cell) was found to be the 3DS-3BS. Differences in the pairing
frequency of the individual chromosome arms of wheat-rye
hybrids have been discussed in relation to the homoeologous
relationships between the constituent genomes of
hexaploid wheat
Response of Wheat Fungal Diseases to Elevated Atmospheric CO2 Level
Infection with fungal pathogens on wheat varieties with different levels of resistance was
tested at ambient (NC, 390 ppm) and elevated (EC, 750 ppm) atmospheric CO2 levels in the
phytotron. EC was found to affect many aspects of the plant-pathogen interaction. Infection
with most fungal diseases was usually found to be promoted by elevated CO2 level in susceptible
varieties. Powdery mildew, leaf rust and stem rust produced more severe symptoms on
plants of susceptible varieties, while resistant varieties were not infected even at EC. The penetration
of Fusarium head blight (FHB) into the spike was delayed by EC in Mv Mambo, while
it was unaffected in Mv Regiment and stimulated in Mv Emma. EC increased the propagation
of FHB in Mv Mambo and Mv Emma. Enhanced resistance to the spread of Fusarium within
the plant was only found in Mv Regiment, which has good resistance to penetration but poor
resistance to the spread of FHB at NC. FHB infection was more severe at EC in two varieties,
while the plants of Mv Regiment, which has the best field resistance at NC, did not exhibit a
higher infection level at EC.
The above results suggest that breeding for new resistant varieties will remain a useful
means of preventing more severe infection in a future with higher atmospheric CO2 levels
Glucocorticoid Receptor-Deficient Foxp3+ Regulatory T Cells Fail to Control Experimental Inflammatory Bowel Disease
Activation of the immune system increases systemic adrenal-derived glucocorticoid (GC) levels which downregulate the immune response as part of a negative feedback loop. While CD4+ T cells are essential target cells affected by GC, it is not known whether these hormones exert their major effects on CD4+ helper T cells, CD4+Foxp3+ regulatory T cells (Treg cells), or both. Here, we generated mice with a specific deletion of the glucocorticoid receptor (GR) in Foxp3+ Treg cells. Remarkably, while basal Treg cell characteristics and in vitro suppression capacity were unchanged, Treg cells lacking the GR did not prevent the induction of inflammatory bowel disease in an in vivo mouse model. Under inflammatory conditions, GR-deficient Treg cells acquired Th1-like characteristics and expressed IFN-gamma, but not IL-17, and failed to inhibit pro-inflammatory CD4+ T cell expansion in situ. These findings reveal that the GR is critical for Foxp3+ Treg cell function and suggest that endogenous GC prevent Treg cell plasticity toward a Th1-like Treg cell phenotype in experimental colitis. When equally active in humans, a rationale is provided to develop GC-mimicking therapeutic strategies which specifically target Foxp3+ Treg cells for the treatment of inflammatory bowel disease
Rapid Regulatory T-Cell Response Prevents Cytokine Storm in CD28 Superagonist Treated Mice
Superagonistic CD28-specific monoclonal antibodies (CD28SA) are highly effective activators of regulatory T-cells (Treg cells) in rats, but a first-in-man trial of the human CD28SA TGN1412 resulted in an unexpected cytokine release syndrome. Using a novel mouse anti-mouse CD28SA, we re-investigate the relationship between Treg activation and systemic cytokine release. Treg activation by CD28SA was highly efficient but depended on paracrine IL-2 from CD28SA-stimulated conventional T-cells. Systemic cytokine levels were innocuous, but depletion of Treg cells prior to CD28SA stimulation led to systemic release of proinflammatory cytokines, indicating that in rodents, Treg cells effectively suppress the inflammatory response. Since the human volunteers of the TGN1412 study were not protected by this mechanism, we also tested whether corticosteroid prophylaxis would be compatible with CD28SA induced Treg activation. We show that neither the expansion nor the functional activation of Treg cells is affected by high-dose dexamethasone sufficient to control systemic cytokine release. Our findings warn that preclinical testing of activating biologicals in rodents may miss cytokine release syndromes due to the rapid and efficacious response of the rodent Treg compartment, and suggest that polyclonal Treg activation is feasible in the presence of antiphlogistic corticosteroid prophylaxis
Temporal Pattern of ICAM-I Mediated Regulatory T Cell Recruitment to Sites of Inflammation in Adoptive Transfer Model of Multiple Sclerosis
Migration of immune cells to the target organ plays a key role in autoimmune disorders like multiple sclerosis (MS). However, the exact underlying mechanisms of this active process during autoimmune lesion pathogenesis remain elusive. To test if pro-inflammatory and regulatory T cells migrate via a similar molecular mechanism, we analyzed the expression of different adhesion molecules, as well as the composition of infiltrating T cells in an in vivo model of MS, adoptive transfer experimental autoimmune encephalomyelitis in rats. We found that the upregulation of ICAM-I and VCAM-I parallels the development of clinical disease onset, but persists on elevated levels also in the phase of clinical remission. However, the composition of infiltrating T cells found in the developing versus resolving lesion phase changed over time, containing increased numbers of regulatory T cells (FoxP3) only in the phase of clinical remission. In order to test the relevance of the expression of cell adhesion molecules, animals were treated with purified antibodies to ICAM-I and VCAM-I either in the phase of active disease or in early remission. Treatment with a blocking ICAM-I antibody in the phase of disease progression led to a milder disease course. However, administration during early clinical remission aggravates clinical symptoms. Treatment with anti-VCAM-I at different timepoints had no significant effect on the disease course. In summary, our results indicate that adhesion molecules are not only important for capture and migration of pro-inflammatory T cells into the central nervous system, but also permit access of anti-inflammatory cells, such as regulatory T cells. Therefore it is likely to assume that intervention at the blood brain barrier is time dependent and could result in different therapeutic outcomes depending on the phase of CNS lesion development
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