scholarly journals Morphological characteristic of inguinal lymph nodes in HIV infection

2019 ◽  
Vol 36 (2) ◽  
pp. 51-59
Author(s):  
N. I. Gulyaeva ◽  
G. G. Freind ◽  
N. G. Shmagel ◽  
L. B. Korolevskaya ◽  
E. V. Saidakova ◽  
...  

Aim. To assess the morphological changes in inguinal lymph nodes among patients with stage 4a HIV infection, who receive antiretroviral therapy. Materials and methods. There were examined 12 HIV-infected patients with stage 4a, treated at “Perm Regional Center for Prevention and Fight against AIDS and Infectious Diseases”, who received antiretroviral therapy for 2 years. Two groups of patients were formed: group I – 6 persons, whose CD+ blood lymphocyte number was more than 350 in 1 mcl; group II – 6 persons with CD+ blood lymphocyte number less than 350 in 1 mcl. Inguinal lymph nodes (ILN) were taken under local anesthesia, histological preparations were prepared by traditional scheme, stained with hematoxylin and eosin using Masson three-colour staining. In immunohistochemical reactions expression of Ki-67 and CD+ markers was estimated. Results.Histoarchitectonics of lymph nodes was changed as a result of massive development of sclerosis in the region of hilum, capsule and trabecules. Against the background of sclerosis, there occurred lymphocyte depletion, change in structure of stromal cells and neoangiogenesis in all the zones of the lymph node. In the regions of sclerosis, death of lymphocytes was revealed. In patients of the second group, more active development of follicles with the centers of reproduction in the lymph node cortical substance, as well as growth of the number of Ki-67 maker-expressing cells was established Conclusions.In the inguinal lymph nodes, the development of sclerotic processes causes the death of T-lymphocytes, which, in their turn, are the source of lymphotoxin-β formation. Loss of CD+-T-lymphocytes is accompanied by deficit of lymphotoxin-β and induces the loss of fibroblastic reticular cells themselves, which through the production of IL-7 support the vital activity of T-cells.

1988 ◽  
Vol 68 (3) ◽  
pp. 474-477 ◽  
Author(s):  
G. W. P. M. Kramer ◽  
E. Rutten ◽  
J. Sloof

✓ A patient with a subcutaneous sacrococcygeal ependymoma and metastasis to the inguinal lymph nodes is presented and his treatment is described. Previous reports on sacrococcygeal ependymoma are reviewed.


2006 ◽  
Vol 32 ◽  
pp. S33
Author(s):  
M. Matter ◽  
D. Liénard ◽  
O. Gugerli ◽  
A. Boubaker ◽  
M. Alloua ◽  
...  

2006 ◽  
Vol 16 (Supplement 1) ◽  
pp. S89
Author(s):  
M. Matter ◽  
D. Li??nard ◽  
O. Gugerli ◽  
A. Boubaker ◽  
M. Alloua ◽  
...  

2016 ◽  
Vol 90 (15) ◽  
pp. 6699-6708 ◽  
Author(s):  
Emily K. Cartwright ◽  
David Palesch ◽  
Maud Mavigner ◽  
Mirko Paiardini ◽  
Ann Chahroudi ◽  
...  

ABSTRACTTreatment of human immunodeficiency virus (HIV) infection with antiretroviral therapy (ART) has significantly improved prognosis. Unfortunately, interruption of ART almost invariably results in viral rebound, attributed to a pool of long-lived, latently infected cells. Based on their longevity and proliferative potential, CD4+T memory stem cells (TSCM) have been proposed as an important site of HIV persistence. In a previous study, we found that in simian immunodeficiency virus (SIV)-infected rhesus macaques (RM), CD4+TSCMare preserved in number but show (i) a decrease in the frequency of CCR5+cells, (ii) an expansion of the fraction of proliferating Ki-67+cells, and (iii) high levels of SIV DNA. To understand the impact of ART on both CD4+TSCMhomeostasis and virus persistence, we conducted a longitudinal analysis of these cells in the blood and lymph nodes of 25 SIV-infected RM. We found that ART induced a significant restoration of CD4+CCR5+TSCMboth in blood and in lymph nodes and a reduction in the fraction of proliferating CD4+Ki-67+TSCMin blood (but not lymph nodes). Importantly, we found that the level of SIV DNA in CD4+transitional memory (TTM) and effector memory (TEM) T cells declined ∼100-fold after ART in both blood and lymph nodes, while the level of SIV DNA in CD4+TSCMand central memory T cells (TCM-) did not significantly change. These data suggest that ART is effective at partially restoring CD4+TSCMhomeostasis, and the observed stable level of virus in TSCMsupports the hypothesis that these cells are a critical contributor to SIV persistence.IMPORTANCEUnderstanding the roles of various CD4+T cell memory subsets in immune homeostasis and HIV/SIV persistence during antiretroviral therapy (ART) is critical to effectively treat and cure HIV infection. T memory stem cells (TSCM) are a unique memory T cell subset with enhanced self-renewal capacity and the ability to differentiate into other memory T cell subsets, such as central and transitional memory T cells (TCMand TTM, respectively). CD4+TSCMare disrupted but not depleted during pathogenic SIV infection. We find that ART is partially effective at restoring CD4+TSCMhomeostasis and that SIV DNA harbored within this subset contracts more slowly than virus harbored in shorter-lived subsets, such as TTMand effector memory (TEM). Because of their ability to persist long-term in an individual, understanding the dynamics of virally infected CD4+TSCMduring suppressive ART is important for future therapeutic interventions aimed at modulating immune activation and purging the HIV reservoir.


AIDS ◽  
1997 ◽  
Vol 11 (9) ◽  
pp. 1103-1110 ◽  
Author(s):  
Hans-Jürgen Stellbrink ◽  
Jan van Lunzen ◽  
Frank T. Hufert ◽  
Günter Fröschle ◽  
Guido Wolf-Vorbeck ◽  
...  

1999 ◽  
Vol 73 (2) ◽  
pp. 1573-1579 ◽  
Author(s):  
Marcelo J. Kuroda ◽  
Jörn E. Schmitz ◽  
William A. Charini ◽  
Christine E. Nickerson ◽  
Carol I. Lord ◽  
...  

ABSTRACT Most studies of human immunodeficiency virus type 1 (HIV-1)-specific cytotoxic T lymphocytes (CTL) have been confined to the evaluation of these effector cells in the peripheral blood. What has not been clear is the extent to which CTL activity in the blood actually reflects this effector cell function in the lymph nodes, the major sites of HIV-1 replication. To determine the concordance between CTL activity in lymph nodes and peripheral blood lymphocytes (PBL), CTL specific for simian immunodeficiency virus of macaques (SIVmac) have been characterized in lymph nodes of infected, genetically selected rhesus monkeys by using both Gag peptide-specific functional CTL assays and tetrameric peptide-major histocompatibility complex (MHC) class I molecule complex staining techniques. In studies of six chronically SIVmac-infected rhesus monkeys, Gag epitope-specific functional lytic activity and specific tetrameric peptide-MHC class I staining were readily demonstrated in lymph node T lymphocytes. Although the numbers of tetramer-binding cells in some animals differed from those documented in their PBL, the numbers of tetramer-binding cells from these two different compartments were not statistically different. Phenotypic characterization of the tetramer-binding CD8+lymph node T lymphocytes of the infected monkeys demonstrated a high level of expression of the activation-associated adhesion molecules CD11a and CD49d, the Fas molecule CD95, and MHC class II-DR. These studies documented a low expression of the naive T-cell marker CD45RA and the adhesion molecule CD62L. This phenotypic profile of the tetramer-binding lymph node CD8+ T cells was similar to that of tetramer-binding CD8+ T cells from PBL. These observations suggest that characterization of AIDS virus-specific CTL activity by sampling of cells in the peripheral blood should provide a reasonable estimation of CTL in an individual’s secondary lymphoid tissue.


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