Recipient�s Reactive Changes of Leucocytes on Sensibilisation by Homologous Tissue Antigens

2015 ◽  
pp. 319-320
Author(s):  
G. P. Kudrina ◽  
P. P. Sakharov
Keyword(s):  
Reactive Changes ◽  
Tissue Antigens ◽  
Homologous Tissue

Reactive changes in leukocytes in animals sensitized with homologous tissue antigens

1969 ◽  
Vol 68 (3) ◽  
pp. 1048-1051
Author(s):  
M. M. Kapichnikov ◽  
P. P. Sakharov ◽  
G. P. Kudrina
Keyword(s):  
Reactive Changes ◽  
Tissue Antigens ◽  
Homologous Tissue

scholarly journals SPLEEN CELL PROLIFERATION IN RESPONSE TO HOMOLOGOUS ANTIGENS STUDIED IN CONGENIC RESISTANT STRAINS OF MICE

1966 ◽  
Vol 123 (4) ◽  
pp. 665-671 ◽  
Author(s):  
Richard W. Dutton
Keyword(s):  
Spleen Cell ◽  
Single Gene ◽  
Inbred Strains ◽  
Histocompatibility Antigens ◽  
Inbred Strains Of Mice ◽  
Tissue Antigens ◽  
Resistant Strains ◽  
The Difference ◽  
Homologous Tissue

The proliferative responses obtained when spleen cell suspensions from two different inbred strains of mice were mixed were investigated further using congenic resistant strain pairs. Strong responses were obtained in 9 cases out of 12 where the two strains differed at a single gene locus controlling an H-2 histocompatibility antigen. No responses were obtained where the difference occurred at loci controlling weak histocompatibility antigens. These findings have been taken to provide additional circumstantial evidence that the response represents an in vitro homograft reaction to homologous tissue antigens.

Antibodies to species homologous tissue antigens in the rat

1968 ◽  
Vol 154 (3) ◽  
pp. 204-209 ◽  
Author(s):  
J. H. Boss ◽  
D. Nelken
Keyword(s):  
Tissue Antigens ◽  
Homologous Tissue

Demonstration of Humoral and Cellular Fixed Antibodies against Homologous Tissue Antigens

Nature ◽  
1963 ◽  
Vol 197 (4865) ◽  
pp. 403-404
Author(s):  
F. SCHEIFFARTH ◽  
H. WARNATZ ◽  
W. FRENGER
Keyword(s):  
Tissue Antigens ◽  
Homologous Tissue

Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

1995 ◽  
Vol 53 ◽  
pp. 958-959
Author(s):  
S.S. Spicer ◽  
B.A. Schulte
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Peripheral Nervous System ◽  
Sensory Neurons ◽  
Sensory Nerves ◽  
Tissue Antigens ◽  
The Central Nervous System ◽  
The Brain ◽  
Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

Testosterone-dependent changes in neurons of hypothalamic arcuate nucleus and reversibility of these changes by modeled male hypogonadism

2017 ◽  
pp. 21-30
Author(s):  
А.В. Дробленков ◽  
Л.Г. Прошина ◽  
Ю.Н. Юхлина ◽  
А.А. Байрамов ◽  
П.Д. Шабанов ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Nerve Cell ◽  
Arcuate Nucleus ◽  
Degenerative Changes ◽  
Control Group ◽  
Male Hypogonadism ◽  
Nissl Staining ◽  
Neuron Body ◽  
Androgen Synthesis ◽  
Reactive Changes

Актуальность. Значение недостаточности тестостерона для структурного гомеостазиса нейронов, регулирующих выработку гонадотропин-рилизинг гормона (ГнРГ) и синтезирующих данный гормон, мало изучены. Цель. Установить реактивные изменения, количество рецепторов к андрогенам (АР) и особенности их распределения в нейронах медиального аркуатного ядра гипоталамуса (МАЯ) при экспериментальном гипогонадизме, а также обратимость этих изменений после восстановительной терапии тестостероном. Методы. У самцов крыс Вистар (16 особей) моделировали гипогонадизм путем удаления одной гонады на 2-3 день постнатальной жизни и исследовали гистологические срезы каудальной части МАЯ у молодых животных (4 мес.) при отсутствии и осуществлении заместительной терапии. Контрольную группу составляли интактные самцы аналогичного возраста (8 особей). В середине левосторонней части МАЯ на площади 0,01 мм определяли реактивные изменения клеток и площадь тел малоизмененных нейронов (после окрашивания срезов методом Ниссля), а также число и долю тел нервных клеток, различавшихся по степени экспрессии АР. Результаты. Установлено, что нейроны МАЯ содержат большое количество АР, распределенных в различных частях их тела. При гипогонадизме происходит перераспределение АР и снижение степени их экспрессии (количества). Сгущение АР в области оболочки ядра и плазмолеммы, образование конгломератов в ядре и цитоплазме было характерно для нейронов с умеренной экспрессией. В цитоплазме и в области плазматической мембраны рецепторы отсутствовали у клеток со слабой и очень низкой экспрессией. Снижение степени экспрессии АР при гипогонадизме сопряжено с уменьшением площади тела и гибелью части нейронов. Заключение. Выявленные дегенеративные тестостерон-зависимые изменения нейронов МАЯ, которые синтезируют ГнРГ или пептиды, влияющие на его выработку, могут обусловить уменьшение высвобождения гонадолиберина, вторичное снижение синтеза андрогенов и реализацию морфофункциональных проявлений его вторичного дефицита. Заместительная терапия частично компенсирует дегенеративные изменения нейронов, восстанавливает интенсивность экспрессии АР, однако не влияет на процесс гибели нервных клеток. Background. Importance of testosterone deficiency for structural homeostasis of the neurons regulating production of gonadotropin-releasing hormone (GnRH) and synthesizing this hormone is insufficiently understood. Aim. To determine reactive changes, quantity of androgens receptors (AR), and features of their distribution in neurons of hypothalamic medial arcuate nucleus (MAN) in experimental hypogonadism and reversibility of these changes by restorative therapy with testosterone. Methods. Hypogonadism was modeled in 16 Wistar rats by removing one gonad on postnatal days 2-3, and histological sections of caudal MAN were examined in young, 4-month old animals with and without a replacement therapy. The control group consisted of 8 age-matched intact males. Cell reactive changes, areas of slightly changed neuron bodies (Nissl staining of sections), and the number and proportion of nerve cell bodies differing in the degree of AR expression were determined in the middle left-sided part of MAN, on an area of 0.01 mm. Results. MAN neurons contained a large quantity of AR distributed in different parts of the neuron body. In hypogonadism, AR redistributed and their expression (quantity) decreased. Condensation of AR in the region of nucleo- and plasmolemma and formation of conglomerates in the nucleus and cytoplasm were characteristic of neurons with moderate expression. In the regions of cytoplasm and plasma membrane, the receptors were absent in cells with low and very low expression. The reduced AR expression in hypogonadism was associated with a decreased neuron body area and death of a part of neurons. Conclusions. The identified degenerative changes in the testosterone-dependent neuronal MAN that synthesize GnRH or peptides affecting the GnRH production may decrease the release of GnRH, cause a secondary decrease in the androgen synthesis, and mediate morphological and functional manifestations of GnRH secondary deficit. The replacement therapy partially compensated for degenerative changes in neurons and restored the intensity of AR expression, however, it did not influence the process of nerve cell death.

scholarly journals STUDIES ON THE IMMUNOTHERAPY OF RUNT DISEASE IN RATS

1969 ◽  
Vol 129 (4) ◽  
pp. 647-661 ◽  
Author(s):  
Willys K. Silvers ◽  
R. E. Billingham
Keyword(s):  
Early Stage ◽  
Fatal Outcome ◽  
Dosage Level ◽  
Cell Suspensions ◽  
Necessary Condition ◽  
Target Cells ◽  
Protective Agent ◽  
Cutaneous Manifestations ◽  
Therapeutic Value ◽  
Tissue Antigens

Using rats of the Lewis and BN (Ag-B locus incompatible) isogenic strains, a comparative study has been made of the capacity to prevent or mitigate the development of runt disease with: (a) lymph node cell suspensions from normal adult BN rats, (b) node cells, or (c) serum from donors sensitized against Lewis tissue antigens, or (d) heterologous anti-lymphocyte serum (ALS) raised in rabbits against rat thymocytes. Following a standard intravenous or intraperitoneal inoculation of 20 x 106 Lewis node cells into neonatal BN hosts, there are cutaneous manifestations of runt disease within 11–15 days and death invariably takes place within 20 days. However, complete protection is afforded by administration of a similar number of normal BN node cells via a different vein, or admixed with the otherwise harmful Lewis node cells. However, timing of the administration was crucially important—precedence or delay by as little as 4 hr resulted in a great impairment of protection. When the inoculations of the two cell suspensions were separated by 24 hr, no protection was afforded. These and other observations suggested that a necessary condition for protection of the hosts by unsensitized isologous cells requires that they establish a prompt and intimate confrontation with the homologous target cells. At the same dosage level, suspensions of node cells from sensitized isologous donors were much more effective therapeutically, saving the lives of 92% of treated subjects when administered after a delay of 3 days, and of 19% when the delay was 4 or 5 days. Of the various immunotherapeutic agents studied, daily injections of 0.2 ml of isoantiserum gave the best results, and could totally reverse the course of the disease even when initiated at age 10–13 days and subjects already presented symptoms. ALS, although inferior to isoantiserum at the dosage levels tested, proved to be superior to sensitized isologous cells as a protective agent, since the initiation of daily injections after delays of 6 or 8 days were still effective. The observations that delayed treatments of infant rats with isoantisera or ALS resulted in complete recoveries sustain the thesis that the lesions responsible for the fatal outcome of runt diseases are not inflicted at a very early stage. The efficacy of both isoantisera and ALS as a means of inhibiting the progression of homologous disease also suggests that they may have therapeutic value in situations where this condition is encountered.

Sign in / Sign up

Export Citation Format

Share Document