TY  - JOUR
AB  - Fibroblastic stromal cells are as diverse, in origin and function, as the niches they fashion in the mammalian body. This cellular variety impacts the spectrum of responses elicited by the immune system. Fibroblast influence on the immune system keeps evolving our perspective on fibroblast roles and functions beyond just a passive structural part of organs. This review discusses the foundations of fibroblastic stromal-immune crosstalk, under the scope of stromal heterogeneity as a basis for tissue-specific tutoring of the immune system. Focusing on the skin as a relevant immunological organ, we detail the complex interactions between distinct fibroblast populations and immune cells that occur during homeostasis, injury repair, scarring, and disease. We further review the relevance of fibroblastic stromal cell heterogeneity and how this heterogeneity is central to regulate the immune system from its inception during embryonic development into adulthood.
AU  - Correa-Gallegos, D.
AU  - Jiang, D.
AU  - Rinkevich, Y.
C1  - 62146
C2  - 50667
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
SP  - 147-162
TI  - Fibroblasts as confederates of the immune system.
JO  - Immunol. Rev.
VL  - 302
IS  - 1
PB  - Wiley
PY  - 2021
SN  - 0105-2896
ER  - 

TY  - JOUR
AB  - Immunological Reviews Published by John Wiley & Sons Ltd. Radiotherapy—despite being a local therapy that meanwhile is characterized by an impressively high degree of spatial accuracy—can stimulate systemic phenomena which occasionally lead to regression and rejection of non-irradiated, distant tumor lesions. These abscopal effects of local irradiation have been observed in sporadic clinical case reports since the beginning of the 20th century, and extensive preclinical work has contributed to identify systemic anti-tumor immune responses as the underlying driving forces. Although abscopal tumor regression still remains a rare event in the radiotherapeutic routine, increasing numbers of cases are being reported, particularly since the clinical implementation of immune checkpoint inhibiting agents. Accordingly, interests to systematically exploit the therapeutic potential of radiotherapy-stimulated systemic responses are constantly growing. The present review briefly delineates the history of radiotherapy-induced abscopal effects and the activation of systemic anti-tumor immune responses by local irradiation. We discuss preclinical and clinical reports with specific focus on the corresponding controversies, and we propose issues that should be addressed in the future in order to narrow the gap between preclinical knowledge and clinical experiences.
AU  - Brix, N.*
AU  - Tiefenthaller, A.*
AU  - Anders, H.J.*
AU  - Belka, C.
AU  - Lauber, K.
C1  - 52152
C2  - 43779
CY  - Hoboken
SP  - 249-279
TI  - Abscopal, immunological effects of radiotherapy: Narrowing the gap between clinical and preclinical experiences.
JO  - Immunol. Rev.
VL  - 280
IS  - 1
PB  - Wiley
PY  - 2017
SN  - 0105-2896
ER  - 

TY  - JOUR
AB  - Post-transcriptional gene regulation by RNA-binding proteins is a fast and effective way to adapt gene expression and change cellular responses. These trans-acting factors have been involved in a number of cell fate decisions, and their mutation is often associated with the development of disease. The RNA-binding protein Roquin-1 has been found to be crucial in the maintenance of peripheral tolerance and the prevention of autoimmune disease. This review describes the molecular role of Roquin family proteins in the control of follicular T-helper cell differentiation. Here, we discuss the redundant regulation of Icos and Ox40 costimulatory receptor mRNAs by Roquin-1 and Roquin-2 proteins. A major focus is placed on the distinct activity of Roquin-1 or Roquin-2 proteins in the mouse models of conditional gene targeting. These recent data are then integrated into an interpretation of altered Roquin protein function in the sanroque mouse that expresses the Roquin-1 protein with just one amino acid substitution and, different from the Roquin-1-deficient mouse, develops lupus-like autoimmune disease.
AU  - Heissmeyer, V.
AU  - Vogel, K.U.
C1  - 23705
C2  - 31248
SP  - 273-289
TI  - Molecular control of Tfh-cell differentiation by Roquin family proteins.
JO  - Immunol. Rev.
VL  - 253
IS  - 1
PB  - Wiley-Blackwell
PY  - 2013
SN  - 0105-2896
ER  - 

TY  - JOUR
AB  - Signaling through lymphocyte antigen receptors has the potential to 
      initiate several distinct outcomes: proliferation, differentiation, 
      apoptosis, or functional unresponsiveness. Expansion and differentiation
       of effector T cells is required for defense against foreign antigens, 
      whereas functional unresponsiveness, termed anergy, is a cell-intrinsic 
      mechanism that contributes to peripheral self-tolerance. Other 
      mechanisms of peripheral tolerance include the 'dominant' tolerance 
      imposed by regulatory T cells and immunosuppression mediated by 
      interleukin-10 and transforming growth factor-beta. T- and B-cell 
      antigen receptor ligation induces an increase in intracellular calcium 
      levels as well as activating additional signaling pathways that are 
      further potentiated by costimulatory receptors. In this review, we argue
       that cell-intrinsic programs of peripheral anergy and tolerance are 
      imposed by sustained calcium signaling in lymphocytes. We address in 
      particular the role of the calcium-dependent transcription factor 
      nuclear factor for activation of T cells, which is activated by antigen 
      receptor stimulation and, depending on the presence or absence of input 
      from its transcriptional partner, activator protein-1, dictates two 
      distinct transcriptional programs: activation or tolerance.
AU  - Borde, M.*
AU  - Barrington, R.A.*
AU  - Heissmeyer, V.
AU  - Carroll, M.C.*
AU  - Rao, A.*
C1  - 3076
C2  - 23879
SP  - 105-119
TI  - Transcriptional basis of lymphocyte tolerance.
JO  - Immunol. Rev.
VL  - 210
PY  - 2006
SN  - 0105-2896
ER  -