Peripheral Lymphoid Organ

2016 ◽  
Author(s):  
Douglas M. Templeton ◽  
Michael Schwenk ◽  
Reinhild Klein ◽  
John H. Duffus
Keyword(s):  
Lymphoid Organ ◽  
Peripheral Lymphoid Organ

scholarly journals Effect of Coxsackievirus B4 Infection on the Thymus: Elucidating Its Role in the Pathogenesis of Type 1 Diabetes

2021 ◽  
Vol 9 (6) ◽  
pp. 1177
Author(s):  
Abdulaziz Alhazmi ◽  
Magloire Pandoua Nekoua ◽  
Hélène Michaux ◽  
Famara Sane ◽  
Aymen Halouani ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
T Cell ◽  
Viral Infections ◽  
Lymphoid Organ ◽  
Thymic Epithelial Cells ◽  
Central Tolerance ◽  
Coxsackievirus B4

The thymus gland is a primary lymphoid organ for T-cell development. Various viral infections can result in disturbance of thymic functions. Medullary thymic epithelial cells (mTECs) are important for the negative selection of self-reactive T-cells to ensure central tolerance. Insulin-like growth factor 2 (IGF2) is the dominant self-peptide of the insulin family expressed in mTECs and plays a crucial role in the intra-thymic programing of central tolerance to insulin-secreting islet β-cells. Coxsackievirus B4 (CVB4) can infect and persist in the thymus of humans and mice, thus hampering the T-cell maturation and differentiation process. The modulation of IGF2 expression and protein synthesis during a CVB4 infection has been observed in vitro and in vivo in mouse models. The effect of CVB4 infections on human and mouse fetal thymus has been studied in vitro. Moreover, following the inoculation of CVB4 in pregnant mice, the thymic function in the fetus and offspring was disturbed. A defect in the intra-thymic expression of self-peptides by mTECs may be triggered by CVB4. The effects of viral infections, especially CVB4 infection, on thymic cells and functions and their possible role in the pathogenesis of type 1 diabetes (T1D) are presented.

scholarly journals Regulation by Chemokines of Circulating Dendritic Cell Precursors, and the Formation of Portal Tract–Associated Lymphoid Tissue, in a Granulomatous Liver Disease

2000 ◽  
Vol 193 (1) ◽  
pp. 35-50 ◽  
Author(s):  
Hiroyuki Yoneyama ◽  
Kenjiro Matsuno ◽  
Yanyun Zhang ◽  
Masako Murai ◽  
Meiji Itakura ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Lymphoid Tissue ◽  
Propionibacterium Acnes ◽  
Portal Tract ◽  
Lymphoid Organ ◽  
Solid Organ ◽  
Granulomatous Reaction ◽  
Portal Area ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

We have studied the recruitment and roles of distinct dendritic cell (DC) precursors from the circulation into Propionibacterium acnes–induced granulomas in mouse liver. During infection, F4/80−B220−CD11c+ DC precursors appeared in the circulation, migrated into the perisinusoidal space, and matured within newly formed granulomas. Recruited DCs later migrated to the portal area to interact with T cells in what we term “portal tract–associated lymphoid tissue” (PALT). Macrophage inflammatory protein 1α attracted blood DC precursors to the sinusoidal granuloma, whereas secondary lymphoid organ chemokine (SLC) attracted mature DCs to the newly identified PALT. Anti-SLC antibody diminished PALT expansion while exacerbating granuloma formation. Therefore, circulating DC precursors can migrate into a solid organ like liver, and participate in the granulomatous reaction in response to specific chemokines.

scholarly journals Enhanced Antigen-Specific Delayed-Type Hypersensitivity and Immunoglobulin G2b Responses after Oral Administration of ViableLactobacillus casei YIT9029 in Wistar and Brown Norway Rats

2001 ◽  
Vol 8 (4) ◽  
pp. 762-767 ◽  
Author(s):  
R. de Waard ◽  
J. Garssen ◽  
J. Snel ◽  
G. C. A. M. Bokken ◽  
T. Sako ◽  
...  
Keyword(s):  
Trichinella Spiralis ◽  
Active Role ◽  
Lymphoid Organ ◽  
Delayed Type Hypersensitivity ◽  
Brown Norway ◽  
Infection Model ◽  
Cell Mediated Immunity ◽  
Th1 Cell ◽  
Inflammatory Reactions ◽  
Norway Rats

ABSTRACT In this study, the effects of orally administered viableLactobacillus casei Shirota strain YIT9029 on the immunity parameters of Wistar and Brown Norway rats were examined. For this purpose, we used the Trichinella spiralis host resistance model. Two weeks before and during T. spiralisinfection, rats were fed 109 viable L. casei bacteria 5 days per week. The T. spiralis-specific delayed-type hypersensitivity (DTH) response was significantly enhanced in both Wistar and Brown Norway rats given L. casei. In both rat strains fedL. casei, serum T. spiralis-specific immunoglobulin G2b (IgG2b) concentrations were also significantly increased. In the model, no significant effects ofL. casei on larval counts or inflammatory reactions in the tongue musculature, body weights, or lymphoid organ weights were observed. Serum specific antibody responses, other than IgG2b, were not changed by feeding of L. casei. In contrast toL. casei, it was shown that orally administeredBifidobacterium breve or Bifidobacterium bifidum had no influence on the measured infection and immunity indices in the rat infection model. Since the rat DTH response is considered to be a manifestation of Th1 cell-mediated immunity and the IgG2b isotype has been associated with Th1 activity, it was concluded that Th1 cells could play an active role in the immunomodulatory effects of orally administered L. casei. Furthermore, our data do not indicate that the effect of oral supplementation withL. casei is dependent on the genetic background of the host.

scholarly journals The thymus and the science of self

2021 ◽  
Author(s):  
Vincent Geenen
Keyword(s):  
T Cells ◽  
Adaptive Immune System ◽  
Lymphoid Organ ◽  
The Body ◽  
Effector Cells ◽  
Major Organ ◽  
Organ Specific ◽  
Health And Disease ◽  
Essential State ◽  
The 1960S

AbstractThe conventional perception asserts that immunology is the science of ‘discrimination’ between self and non-self. This concept is however no longer tenable as effector cells of the adaptive immune system are first conditioned to be tolerant to the body’s own antigens, collectively known as self until now. Only then attain these effectors the responsiveness to non-self. The acquisition of this essential state of tolerance to self occurs for T cells in the thymus, the last major organ of our body that revealed its intricate function in health and disease. The ‘thymus’ as an anatomical notion was first notably documented in Ancient Greece although our present understanding of the organ’s functions was only deciphered commencing in the 1960s. In the late 1980s, the thymus was identified as the site where clones of cells reactive to self, termed ‘forbidden’ thymocytes, are physically depleted as the result of a process now known as negative selection. The recognition of this mechanism further contributed to the belief that the central rationale of immunology as a science lies in the distinction between self and non-self. This review will discuss the evidence that the thymus serves as a unique lymphoid organ able to instruct T cells to recognize and be tolerant to harmless self before adopting the capacity to defend the body against potentially injurious non-self-antigens presented in the context of different challenges from infections to exposure to malignant cells. The emerging insight into the thymus’ cardinal functions now also provides an opportunity to exploit this knowledge to develop novel strategies that specifically prevent or even treat organ-specific autoimmune diseases.

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