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001-es BibID:BIBFORM046529
Első szerző:Gonda Andrea (onkológus szakorvos)
Cím:CD44, but not l-selectin, is critically involved in leucocyte migration into the skin in a murine model of allergic dermatitis / Gonda A., Gal I., Szanto S., Sarraj B., Glant T. T., Hunyadi J., Mikecz K.
Dátum:2005
ISSN:0906-6705
Megjegyzések:CD44 and l-selectin (CD62L) are major adhesion receptors that mediate leucocyte recruitment at inflammatory sites and lymph nodes, by supporting cell rolling under blood flow. Both CD44 and CD62L have been implicated in inflammatory skin disorders, but their specific involvement in an immediate-type allergic reaction remains uncertain. We used mice deficient in CD44 or CED62L or both in order to determine whether one or both of these molecules were required for leucocyte extravasation in an atopic dermatitis-like allergic response. Wild-type (WT) mice and mice deficient in CD44, CD62L or both were immunized with ovalbumin (OVA). Inflammatory reaction in the ear was elicited once by means of intradermal injection of OVA. Effective sensitization of CD62L knockout (KO) mice required intraperitoneal antigen injection; however, OVA-specific T helper 2 (Th2)-type immune responses and IgE production in mice lacking CD44, CD62L or both were comparable to those in WT mice following intraperitoneal immunization. We employed intravital videomicroscopy to monitor the recruitment of fluorescence-labelled leucocytes to the ear tissue following challenge with OVA. The number of adherent leucocytes was significantly reduced in CD44 KO and CD44/CD62L double KO mice, indicating that CD44 was involved in firm adhesion, the committed step of leucocyte extravasation. Histology of the OVA-challenged ears showed a diminished leucocyte infiltration in the ears of CD44 KO and double KO mice. The results of our study demonstrate that CD44, but not CD62L, is required for leucocyte extravasation during a Th2-type inflammatory response.újratöltve - BIBFORM015941
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
allergic dermatitis
CD44
CD62L
intravital videomicroscopy
leucocyte migration
Megjelenés:Experimental Dermatology. - 14 : 9 (2005), p. 700-708. -
További szerzők:Gál István (1957-) (belgyógyász) Szántó Sándor (1968-) (belgyógyász, reumatológus) Sarraj, Bara Glant Tibor T. Hunyadi János (1943-) (bőrgyógyász, kozmetológus, allergológus) Mikecz Katalin
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2.

001-es BibID:BIBFORM015783
Első szerző:Nesterovitch, Andrew B.
Cím:Spontaneous insertion of a B2 element in the ptpn6 gene drives a systemic autoinflammatory disease in mice resembling neutrophilic dermatosis in humans / Andrew B. Nesterovitch, Sandor Szanto, Andrea Gonda, Tamas Bardos, Katalin Kis-Toth, Vyacheslav A. Adarichev, Katalin Olasz, Sheida Ghassemi-Nejad, Mark D. Hoffman, Michael D. Tharp, Katalin Mikecz, Tibor T. Glant
Dátum:2011
ISSN:0002-9440
Megjegyzések:We found a spontaneous autosomal mutation in a mouse leading to neutrophil infiltration with ulceration in the upper dermis of homozygous offspring. These animals had increased neutrophil numbers, associated with normal lymphocyte count, in peripheral blood and bone marrow, suggesting a myeloproliferative disorder; however, granulocyte precursor proliferation in bone marrow was actually reduced (because circulating neutrophils were less susceptible to apoptosis). Neutrophil infiltration of the skin and other organs and high serum levels of immunoglobulins and autoantibodies, cytokines, and acute-phase proteins were additional abnormalities, all of which could be reduced by high-dose corticosteroid treatment or neutrophil depletion by antibodies. Use of genome-wide screening localized the mutation within an 0.4-Mbp region on mouse chromosome 6. We identified insertion of a B2 element in exon 6 of the Ptpn6 gene (protein tyrosine phosphatase, non-receptor type 6; also known as Shp-1). This insertion involves amino acid substitutions that significantly reduced the enzyme activity in mice homozygous for the mutation. Disease onset was delayed, and the clinical phenotype was milder than the phenotypes of other Ptpn6-mutants described in motheaten (me, mev) mice; we designated this new genotype as Ptpn6(meB2/meB2) and the phenotype as meB2. This new phenotype encompasses an autoinflammatory disease showing similarities to many aspects of the so-called neutrophilic dermatoses, a heterogeneous group of skin diseases with unknown etiology in humans.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Pathology 178 : 4 (2011), p. 1701-1714. -
További szerzők:Szántó Sándor (1968-) (belgyógyász, reumatológus) Gonda Andrea (1970-) (onkológus szakorvos) Bárdos Tamás Kis-Tóth Katalin (1975-) (immunológus) Adarichev, Vyacheslav A. Olasz Katalin Ghassemi-Nejad, Sheida (1980-) (fogorvos) Hoffman, Mark D. Tharp, Michael D. Mikecz Katalin Glant Tibor T.
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
elektronikus elérés
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3.

001-es BibID:BIBFORM046534
Első szerző:Szántó Sándor (belgyógyász, reumatológus)
Cím:Expression of L-selectin, but not CD44, is required for early neutrophil extravasation in antigen-induced arthritis / Sándor Szántó, István Gál, Andrea Gonda, Tibor T. Glant, Katalin Mikecz
Dátum:2004
Megjegyzések:L (leukocyte)-selectin (CD62L) and CD44 are major adhesion receptors that support the rolling of leukocytes on endothelium, the first step of leukocyte entry into inflamed tissue. The specific contribution of L-selectin or CD44 to the regulation of cell traffic to joints in arthritis has not been investigated. We used CD44-deficient, L-selectin-deficient, and CD44/L-selectin double knockout mice to determine the requirement for these receptors for inflammatory cell recruitment during Ag-induced arthritis. Intraperitoneal immunization resulted in similar activation status and Ag-specific responses in wild-type and gene-targeted mice. However, extravasation of neutrophil granulocytes, but not the emigration of T cells, into the knee joints after intra-articular Ag injection was significantly delayed in L-selectin-deficient and double knockout mice. Intravital videomicroscopy on the synovial microcirculation revealed enhanced leukocyte rolling and diminished adherence in mice lacking either CD44 or L-selectin, but CD44 deficiency had no significant effect on the recruitment of L-selectin-null cells. Compared with wild-type leukocytes, expression of L-selectin was down-regulated in CD44-deficient cells in the spleen, peripheral blood, and inflamed joints, suggesting that reduced expression of L-selectin, rather than the lack of CD44, could be responsible for the delayed influx of granulocytes into the joints of CD44-deficient mice. In conclusion, there is a greater requirement for L-selectin than for CD44 for neutrophil extravasation during the early phase of Ag-induced arthritis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Immunology. - 172 : 11 (2004), p. 6723-6734. -
További szerzők:Gál István (1957-) (belgyógyász) Gonda Andrea (1970-) (onkológus szakorvos) Glant Tibor T. Mikecz Katalin
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