scholarly journals Adaptive Immune Deficiency Impairs Neural Activity After Training and Retrieval

2021 ◽  
Vol 15 ◽  
Author(s):  
Huiping Li ◽  
Zhongxiao Fu ◽  
Meixin Hu ◽  
Xiu Xu
Keyword(s):  
Immune Deficiency ◽  
Adaptive Immunity ◽  
Neural Activity ◽  
Neurodevelopmental Disorders ◽  
Brain Regions ◽  
Scid Mice ◽  
Contextual Fear Conditioning ◽  
Severe Combined Immune Deficiency ◽  
Neuronal Function ◽  
Adaptive Immune

Neuroimmune interactions have been studied for decades. Several neurodevelopmental disorders have been associated with immune dysfunction. However, the effects of immune system on neuronal function remain unknown. Herein, based on c-Fos protein expression, we characterized the brain areas that are activated after contextual fear conditioning (CFC) training or retrieval in severe combined immune deficiency (SCID) and wild-type mice. Further, we analyzed the interregional correlations of c-Fos activity that are affected by deficiency in adaptive immunity. Results showed significantly lower c-Fos density in learning and memory-associated brain regions of SCID mice after memory retrieval, but not during the CFC training. Moreover, SCID mice exhibited remarkably discordant interregional neuronal activities of learning neuron circuits after CFC training, which could be the cause of inefficient activation of the memory circuit after retrieval. These results provide a new perspective on how adaptive immunity affects neuronal function. Adaptive immune deficiency impairs the coordination of neural activity after training and retrieval, which might be a potential therapeutic target for neurodevelopmental disorders.

scholarly journals Rejection of bone marrow allografts by mice with severe combined immune deficiency (SCID). Evidence that natural killer cells can mediate the specificity of marrow graft rejection.

1987 ◽  
Vol 165 (4) ◽  
pp. 1212-1217 ◽  
Author(s):  
W J Murphy ◽  
V Kumar ◽  
M Bennett
Keyword(s):  
Immune Deficiency ◽  
Nk Cells ◽  
Natural Killer ◽  
Cell Function ◽  
Scid Mice ◽  
Severe Combined Immune Deficiency ◽  
Marrow Graft ◽  
Specific Receptors ◽  
Combined Immune Deficiency ◽  
Allogeneic Marrow

C.B-17 scid (H-2d) mice are homozygous for the gene that causes severe combined immune deficiency (SCID). These mice have no T or B cell function, yet display normal natural killer (NK) activity. Irradiated SCID mice were challenged with marrow grafts to determine if antibodies are necessary for marrow allograft rejection. SCID mice rejected H-2/Hh-1 allogeneic marrow grafts. Moreover, this rejection capability could be adoptively transferred using SCID marrow as a source of NK progenitors infused into irradiated B6 (H-2b) hosts. We conclude that NK cells can mediate marrow allograft reactivity in the absence of immunoglobulin. It follows that NK cells probably have specific receptors for Hh antigens.

scholarly journals Seeding Efficiency of Primitive Human Hematopoietic Cells in Nonobese Diabetic/Severe Combined Immune Deficiency Mice: Implications for Stem Cell Frequency Assessment

Blood ◽  
1999 ◽  
Vol 94 (9) ◽  
pp. 3055-3061 ◽  
Author(s):  
Paula B. van Hennik ◽  
Alexandra E. de Koning ◽  
Rob E. Ploemacher
Keyword(s):  
Immune Deficiency ◽  
Stem Cell ◽  
Great Influence ◽  
Cell Subset ◽  
Scid Mice ◽  
Human Umbilical Cord ◽  
Severe Combined Immune Deficiency ◽  
Nonobese Diabetic ◽  
Combined Immune Deficiency ◽  
Seeding Efficiency

Nonobese diabetic/severe combined immune deficiency (NOD/SCID) mouse repopulating cells (SRC) have been proposed to represent a more primitive human stem cell subset than the cobblestone area-forming cell (CAFC) week (wk) 6 or the long-term culture-initiating cell (LTC-IC) wk 5 on the basis of their difference in frequency, phenotype, transfectibility, and multilineage outgrowth potential in immunodeficient recipients. We have assessed the percentage of various progenitor cell populations (colony-forming cell [CFC] and CAFC subsets) contained in unsorted NOD/SCID BM nucleated cells (nc), human umbilical cord blood (UCB) nc, bone marrow (BM) nc, peripheral blood stem cells (PBSC), and CD34+ selected UCB nc, seeding in the BM and spleen of NOD/SCID mice within 24 hours after transplantation. The seeding efficiency of NOD/SCID BM CAFC wk 5 was median (range) in the spleen 2.9% (0.7% to 4.0%) and in the total BM 8.7% (2.0% to 9.2%). For human unsorted UCB nc, BM nc, PBSC, and CD34+ UCB cells, the seeding efficiency for CAFC wk 6 in the BM of NOD/SCID mice was 4.4% (3.5% to 6.3%), 0.8% (0.3% to 1.7%), 5.3% (1.4% to 13.6%), and 4.4% (3.5% to 6.3%), respectively. Using flow cytometry, the percentage CD34+UCB cells retrieved from the BM of sublethally or supralethally irradiated NOD/SCID mice was 2.3 (1.4 to 2.8) and 2.5 (1.6 to 2.7), respectively. Because we did not observe any significant differences in the seeding efficiencies of the various stem cell subsets, it may be assumed that the SRC seeding efficiency in NOD/SCID mice is similarly low. Our data indicate that the seeding efficiency of a graft can be of great influence when assessing stem cell frequencies in in vivo repopulation assays.

Elucidation of mode of retroviral-inhibitory effects of imexon through use of immune competent and severe combined immune deficiency (SCID) mice

1992 ◽  
Vol 17 (3) ◽  
pp. 223-233 ◽  
Author(s):  
John D. Morrey ◽  
Jan R. Mead ◽  
Reed P. Warren ◽  
Kevin M. Okleberry ◽  
Roger A. Burger ◽  
...  
Keyword(s):  
Immune Deficiency ◽  
Scid Mice ◽  
Severe Combined Immune Deficiency ◽  
Inhibitory Effects ◽  
Combined Immune Deficiency

scholarly journals Evidence of functional lymphocytes in some (leaky) scid mice.

1988 ◽  
Vol 167 (3) ◽  
pp. 1016-1033 ◽  
Author(s):  
G C Bosma ◽  
M Fried ◽  
R P Custer ◽  
A Carroll ◽  
D M Gibson ◽  
...  
Keyword(s):  
Immune Deficiency ◽  
T Cells ◽  
General Pattern ◽  
Scid Mice ◽  
Lymphoid Tissues ◽  
Severe Combined Immune Deficiency ◽  
Splenic Cells ◽  
Combined Immune Deficiency ◽  
Lymphocyte Antigens ◽  
High Concentrations

Although the majority of severe combined immune deficiency (scid) mice lack functional lymphocytes, some (2-23%) appear to develop a limited number of B and T cells between 3 and 9 mo old. Most of these leaky scid mice were shown to contain very few clones (less than or equal to 3) of Ig-producing plasmacytes. Clonal progeny were distributed unevenly in the lymphatic tissues and appeared as discrete plasmacytic foci. In many cases, individual clones persisted for several months and produced abnormally high concentrations of Ig that included multiple isotypes. Functional T cells were inferred from the ability of leaky mice to reject allogeneic skin grafts, a T cell-dependent reaction. Interestingly, approximately 40% of leaky mice developed thymic lymphomas. In other respects, leaky mice resembled regular scid mice; e.g., their splenic cells failed to express common lymphocyte antigens (Ly-5[B220], Ly-1) and to proliferate in response to lymphocyte mitogens. Histologically, their lymphoid tissues retained the same general pattern of severe lymphocytic deficiency as scid mice.

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