Rat Peritoneal Mast Cells Present Antigen to a PPD-Specific T Cell Line

Fox, Charity C.; Jewell, Scott D.; Whitacre, Caroline C.

doi:10.1006/cimm.1994.1272

Cited by 93 publications

(66 citation statements)

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“…Secondly, our study, along with earlier studies (16), put into question the suggested ability of mast cells to control or modulate autoimmunity-promoting adaptive immune response (14,46). Mast cell deficiency did not affect the levels of conventional or regulatory T cells, B cells, or dendritic cells in the PLNs; moreover, T-cell activation, much of which had previously been suggested to be associated with mast cell function, was also unaffected by mast cell deficiency (23)(24)(25)(28)(29)(30)(31)(32)(33)(34)(35). Obviously, we refrain from extrapolating negative data obtained in experiments on arthritis, experimental autoimmune encephalomyelitis (16), and T1D (this study) to the potential roles of mast cells in other autoimmune responses or adaptive immunity in general.…”

Section: Discussionmentioning

confidence: 52%

“…Akin to humans, in the universally used nonobese diabetic (NOD) mouse model of T1D, the highest genetic contributor to disease susceptibility maps to the major histocompatibility complex (21,22). In view of the T-cell dependency of this disease and the putative roles of mast cells in the control of T-cell responses, which may occur via direct antigen presentation to either CD4 + or CD8 + T cells (23)(24)(25), by induction of T-cell migration to lymph nodes (26,27), by control of dendritic cell activation and migration to lymph nodes (28)(29)(30)(31), or by control of the Th1 versus Th2 skewing (32)(33)(34)(35), it has been postulated that mast cells are likely important players in the development of T1D (14,15,36).…”

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confidence: 99%

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Type 1 Diabetes in NOD Mice Unaffected by Mast Cell Deficiency

Gutierrez

Schönefeldt

et al. 2014

Diabetes

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Mast cells have been invoked as important players in immune responses associated with autoimmune diseases. Based on in vitro studies, or in vivo through the use of Kit mutant mice, mast cells have been suggested to play immunological roles in direct antigen presentation to both CD4+ and CD8+ T cells, in the regulation of T-cell and dendritic cell migration to lymph nodes, and in Th1 versus Th2 polarization, all of which could significantly impact the immune response against self-antigens in autoimmune disease, including type 1 diabetes (T1D). Until now, the role of mast cells in the onset and incidence of T1D has only been indirectly tested through the use of low-specificity mast cell inhibitors and activators, and published studies reported contrasting results. Our three laboratories have generated independently two strains of mast cell–deficient nonobese diabetic (NOD) mice, NOD.Cpa3Cre/+ (Heidelberg) and NOD.KitW-sh/W-sh (Leuven and Boston), to address the effects of mast cell deficiency on the development of T1D in the NOD strain. Our collective data demonstrate that both incidence and progression of T1D in NOD mice are independent of mast cells. Moreover, analysis of pancreatic lymph node cells indicated that lack of mast cells has no discernible effect on the autoimmune response, which involves both innate and adaptive immune components. Our results demonstrate that mast cells are not involved in T1D in the NOD strain, making their role in this process nonessential and excluding them as potential therapeutic targets.

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Section: Discussionmentioning

confidence: 52%

mentioning

confidence: 99%

Type 1 Diabetes in NOD Mice Unaffected by Mast Cell Deficiency

Gutierrez

Schönefeldt

et al. 2014

Diabetes

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“…T cell-mast cell interactions have been shown to be bidirectional, fulfilling mutually regulatory and/or modulatory roles, including influences on cellular processes such as growth, proliferation/activation, migration, and Ag presentation [7][8][9]. So far, the inductive effect of T cells on mast cell activation and degranulation has been attributed to the biological effects of certain cytokines released from the former.…”

Section: Introductionmentioning

confidence: 99%

Activated T lymphocytes induce degranulation and cytokine production by human mast cells following cell-to-cell contact

Bhattacharyya

Drucker

Reshef

et al. 1998

Journal of Leukocyte Biology

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Activated mast cells reside in close apposition to T cells in some inflammatory processes. In this study, we analyzed whether this close physical proximity affects human mast cell degranulation and cytokine release. Thus HMC-1 human mast cells or primary bone marrow-derived human mast cells were cocultured with activated and with resting T cells. Mast cells cocultured with activated T cells released histamine and ␤-hexosaminidase and produced tumor necrosis factor ␣ (TNF-␣), an effect that peaked at 20 h. Kinetics of histamine release paralleled the formation of heterotypic aggregates. Separation of the two cell populations with a porous membrane prevented mediator release and TNF-␣ production. Addition of the PI3-kinase inhibitor, wortmannin, inhibited the heterotypic adhesion-associated degranulation but not TNF-␣ production. These data thus indicate a novel pathway through which human mast cells are activated to both release granule-associated mediators and to produce cytokines in association with heterotypic adhesion to activated human T cells.

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“…In recent years, the functional participation of mast cells has in addition been recognized in various other immunological processes and during connective tissue turnover. Specifically, evidence has been presented that mast cells can express MHC class II molecules [1][2][3][4] and that they are active antigen presenting cells [3,5,6]. Furthermore, the CD34 þ mast cell precursors, as well as immature and mature mast cells, are capable of phagocytosis and chemotaxis [7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Human Leukaemic (HMC‐1) and Normal Skin Mast Cells Express β2‐Integrins: Characterization of β2‐Integrins and ICAM‐1 on HMC‐1 Cells

et al. 1997

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Weber S, Babina M, Feller G, Henz BM. Human Leukaemic (HMC-1) and Normal Skin Mast Cells Express b2-Integrins: Characterization of b2-Integrins and ICAM-1on HMC-1 Cells. Scand J Immunol 1997;45:471-481 Mast cells are bone marrow-derived, ubiquitous connective tissue resident cells. However, their mechanisms of migration, the distribution of immature and mature cells and their interaction with other inflammatory cells are largely unclarified. Possibly, b2-integrins play an important role in these processes. In the present investigation, the authors studied the expression and regulation of the b2-integrins LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18), p150,95 (CD11c/CD18) and of the LFA-1/Mac-1 counter-receptor intercellular adhesion molecule-1 (ICAM-1; CD54) on leukaemic (HMC-1 cell subclone 5C6) and on normal mature human skin mast cells. The HMC-1 cells clearly expressed CD11a, CD18 and CD54, while expression of CD11b and CD11c was low. The apparent molecular weights were 180 kDa (CD11a), 95 kDa (CD18) and 90 kDa (CD54) as determined by Western blot analysis. Phorbol myristate acetate (PMA) induced a time-and dose-dependent up-regulation of CD11a, CD11b, CD11c, CD18 and CD54 that was inhibited by cycloheximide, suggesting a dependence on de novo protein synthesis. Enhanced expression of CD11a, CD11b, CD11c and CD18 could also be confirmed at the gene level as demonstrated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Increased expression of LFA-1/ICAM-1 in response to PMA was accompanied by strong enhancement of homotypic cell aggregation, suggesting that newly synthesized LFA-1/ICAM-1 is functionally active. In order to determine a physiologically relevant way of mast cell b2-integrin modulation, several cytokines and chemotactic mediators (interleukin-4, IL-4; nerve growth factor b, NGFb; C5a; and leukotriene B4, LTB4) were tested for their influence on adhesion molecule cell surface density. Only LTB4 was shown specifically to up-regulate CD11a and CD18, but not CD11b or CD11c. The presence of CD11a, CD11c and CD18 could be confirmed on a low percentage of normal skin mast cells by immunofluorescence, using a double staining technique. In comparison to normal skin, a significantly higher percentage of CD18 þ mast cells was found in inflammatory dermatoses such as psoriasis vulgaris, atopic dermatitis and lichen planus. Therefore, mast cell b2-integrins possibly play an important role during homing of immature mast cells as well as during the interaction of activated mast cells with other inflammatory cells.

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Rat Peritoneal Mast Cells Present Antigen to a PPD-Specific T Cell Line

Cited by 93 publications

References 0 publications

Type 1 Diabetes in NOD Mice Unaffected by Mast Cell Deficiency

Type 1 Diabetes in NOD Mice Unaffected by Mast Cell Deficiency

Activated T lymphocytes induce degranulation and cytokine production by human mast cells following cell-to-cell contact

Human Leukaemic (HMC‐1) and Normal Skin Mast Cells Express β2‐Integrins: Characterization of β2‐Integrins and ICAM‐1 on HMC‐1 Cells

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