scholarly journals The Immunological Organ Environment Dictates the Molecular and Cellular Pathways of Cytotoxic Antibody Activity

Cell Reports ◽  
2019 ◽  
Vol 29 (10) ◽  
pp. 3033-3046.e4 ◽  
Author(s):  
Sina Gordan ◽  
Heike Albert ◽  
Heike Danzer ◽  
Anja Lux ◽  
Markus Biburger ◽  
...  
1997 ◽  
Vol 6 (2) ◽  
pp. 119-124 ◽  
Author(s):  
Anna Hyc ◽  
Jacek Malejczyk ◽  
Anna Osiecka ◽  
Stanislaw Moskalewski

Rat chondrocytes isolated from the articular–epiphyseal cartilage complex were transplanted into defects prepared in articular cartilage and subchondral bone. Transplants were taken for examination after 3 and 8 wk. Cartilage formed by syngeneic chondrocytes did not evoke formation of infiltrations. Contrary to that, in the vicinity of cartilage produced by allogeneic chondrocytes numerous infiltrating cells were present and cartilage resorption could be observed. Cyclosporine-A (CsA) treatment of recipients of allogeneic chondrocytes only partially suppressed accumulation of infiltrating cells and matrix resorption. Antichondrocyte immune response of chondrocyte graft recipients was studied by evaluation of spleen mononuclear cells (SMC) stimulation in mixed splenocytechondrocyte cultures and by evaluation of antichondrocyte cytotoxic antibodies. No difference in stimulation of SMC from intact rats by syngeneic and allogeneic chondrocytes was observed. Stimulation by allogeneic chondrocytes was slightly but significantly higher in recipients of syngeneic grafts. SMC of allogenic chondrocyte recipients were strongly stimulated by allogeneic chondrocytes. This response was absent in recipients treated with CsA. Spontaneous antichondrocyte cytotoxic antibody activity was detected in intact rats and in recipients of syngeneic grafts. In recipients of allogeneic chondrocytes the antibody response against allogeneic chondrocytes was raised but was statistically not significant owing to the considerable variation in the level of spontaneously occurring antichondrocyte antibodies.


1977 ◽  
Vol 216 (1) ◽  
pp. 39-46 ◽  
Author(s):  
V. Kratzsch ◽  
W. R. Kiessling ◽  
J. Wikstr�m ◽  
D. W. Meyer ◽  
K. Eickhoff ◽  
...  

1974 ◽  
Vol 30 (2) ◽  
pp. 181-181
Author(s):  
R Vanwijck ◽  
M C Moor ◽  
S Malek-Mansour ◽  
P Rustin

Author(s):  
Robert P. Apkarian

A multitude of complex ultrastructural features are involved in endothelial cell (EC) gating and sorting of lipid through capillaries and into steroidogenic cells of the adrenal cortex. Correlative microscopy is necessary to distinguish the structural identity of features involved in specific cellular pathways. In addition to diaphragmed fenestrae that frequently appear in clusters, other 60-80 nm openings; plasmalemma vesicles (PV), channels and pockets fitted with diaphragms of the same dimension, coexist on the thin EC surface. Non-diaphragmed coated pits (CP) (100-120 nm) involved in receptor mediated endocytosis were also present on the EC membrane. The present study employed HRSEM of cryofractured and chromium coated specimens and low voltage HRSTEM of 80 nm thick LX-112 embedded sections stained with 2.0% uranyl acetate. Both preparations were imaged at 25 kV with a Topcon DS-130 FESEM equipped with in-lens stage and STEM detector.HRSEM images of the capillary lumen coated with a lnm continuous fine grain Cr film, provided the ability to scan many openings and resolve (SE-I contrast) the fine structure of diaphragm spokes and central densities (Fig. 1).


2013 ◽  
Vol 55 ◽  
pp. 1-15 ◽  
Author(s):  
Laura E. Gallagher ◽  
Edmond Y.W. Chan

Autophagy is a conserved cellular degradative process important for cellular homoeostasis and survival. An early committal step during the initiation of autophagy requires the actions of a protein kinase called ATG1 (autophagy gene 1). In mammalian cells, ATG1 is represented by ULK1 (uncoordinated-51-like kinase 1), which relies on its essential regulatory cofactors mATG13, FIP200 (focal adhesion kinase family-interacting protein 200 kDa) and ATG101. Much evidence indicates that mTORC1 [mechanistic (also known as mammalian) target of rapamycin complex 1] signals downstream to the ULK1 complex to negatively regulate autophagy. In this chapter, we discuss our understanding on how the mTORC1–ULK1 signalling axis drives the initial steps of autophagy induction. We conclude with a summary of our growing appreciation of the additional cellular pathways that interconnect with the core mTORC1–ULK1 signalling module.


2011 ◽  
Vol 44 (06) ◽  
Author(s):  
NC Gassen ◽  
Y Han ◽  
G Wochnik ◽  
F Holsboer ◽  
T Rein

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