scholarly journals Passive transfer of experimental autoimmune myasthenia by lymph node cells in inbred guinea pigs.

1975 ◽  
Vol 142 (3) ◽  
pp. 785-789 ◽  
Author(s):  
R Tarrab-Hazdi ◽  
A Aharonov ◽  
O Abramsky ◽  
I Yaar ◽  
S Fuchs

Passive transfer of experimental autoimmune myasthenia (EAM) was performed with lymph node cells from donor guinea pigs immunized with purified acetylcholine receptor (AChR) from Torpedo californica. Recipient animals revealed the same clinical signs and electromyographic patterns as observed in actively challenged animals. These phenomena are parallel to the clinical manifestations of the human disease myasthenia gravis, in which cellular response to AChR was recently demonstrated.

1976 ◽  
Vol 144 (3) ◽  
pp. 739-753 ◽  
Author(s):  
J M Lindstrom ◽  
A G Engel ◽  
M E Seybold ◽  
V A Lennon ◽  
E H Lambert

Passive transfer of experimental autoimmune myasthenia gravis (EAMG) was achieved using the gamma globulin fraction and purified IgG from sera of rats immunized with Electrophus electricus (eel) acetylcholine receptor (AChR). This demonstrates the critical role of anti-AChR antibodies in impairing neuromuscular transmission in EAMG. Passive transfer of anti-AChR antibodies from rats with chronic EAMG induced signs of the acute phase of EAMG in normal recipient rats, including invasion of the motor end-plate region by mononuclear inflammatory cells. Clinical, eletrophysiological, histological, and biochemical signs of acute EAMG were observed by 24 h after antibody transfer. Recipient rats developed profound weakness and fatigability, and the posture characteristic of EAMG. Striking weight loss was attributable to dehydration. Recipient rats showed large decreases in amplitude of muscle responses to motor nerve stimulation, and repetitive nerve stimulation induced characteristic decrementing responses. End-plate potentials were not detectable in many muscle fibers, and the amplitudes of miniature end-plate potentials were reduced in the others. Passively transferred EAMG more severely affected the forearm muscles than diaphragm muscles, though neuromuscular transmission was impaired and curare sensitivity was increased in both muscles. Some AChR extracted from the muscles of rats with passively transferred EAMG was found to be complexed with antibody, and the total yield of AChR per rat was decreased. The quantitative decrease in AChR approximately paralleled in time the course of clinical and electrophysiological signs. The amount of AChR increased to normal levels and beyond at the time neuromuscular transmission was improving. The excess of AChR extractable from muscle as the serum antibody level decreased probably represented extrajunctional receptors formed in response to functional denervation caused by phagocytosis of the postsynaptic membrane by macrophages. The amount of antibody required to passively transfer EAMG was less than required to bind all AChR molecules in a rat's musculature. The effectiveness of samll amounts of antibody was probably amplified by the activation of complement and by the destruction of large areas of postsynaptic membrane by phagocytic cells. A self-sustaining autoimmune response to AChR was not provoked in animals with passively transferred EAMG.


1958 ◽  
Vol 107 (1) ◽  
pp. 109-124 ◽  
Author(s):  
S. B. Salvin ◽  

Guinea pigs were injected in the footpads with either purified diphtheria toxoid or recrystallized egg albumin in Freund adjuvant without mycobacteria. Each guinea pig was then skin-tested only once with the specific antigen and bled for antibody determination. After injection of the sensitizing antigen, a latent period occurred during which neither sensitivity nor circulating antibody could be detected. A period of delayed sensitivity followed wherein circulating antibody could not be discerned and which could be transferred by lymph node cells. Ultimately, the Arthus type sensitivity developed, accompanied by circulating antibody. The duration and severity of reactions to homologous antigens during the last 2 phases varied with the antigen and with the dose. An increase in the sensitizing dose decreased the duration of the delayed type of allergy, a decrease in the dose prolonged the delayed type. Inclusion of mycobacterium in the sensitizing inoculum tended to introduce delayed sensitivity earlier and delay the onset of Arthus type sensitivity. When specific precipitate in antibody excess was included with the toxoid in the sensitizing dose, the onset of the Arthus phase was hastened. When lymph nodes from a large number of sensitized donors were removed during the latter part of the latent period, recipients of the cells showed a delayed type sensitivity.


Blood ◽  
1965 ◽  
Vol 25 (6) ◽  
pp. 1009-1013 ◽  
Author(s):  
JOHN J. MILLER ◽  
JUDITH MITCHELL

Abstract Differences in the rates of incorporation of tritiated uridine U-H3 of lymph node cells of different species have been found. Plasma cells from humans, guinea pigs, mice, and rabbits have a higher rate of incorporation of U-H3 than do plasma cells from rats, whereas human blast cells have a lower rate of U-H3 incorporation than blast cells from the various rodents.


2010 ◽  
Vol 105 (3) ◽  
pp. 263-268 ◽  
Author(s):  
Juliana Seger ◽  
Sofia Fernanda Gonçalves Zorzella-Pezavento ◽  
Ana Cláudia Pelizon ◽  
Douglas Rodrigues Martins ◽  
Alexandre Domingues ◽  
...  

1983 ◽  
Vol 157 (6) ◽  
pp. 2087-2096 ◽  
Author(s):  
W A Sewell ◽  
J J Munoz ◽  
M A Vadas

Pertussigen, a purified protein from Bordetella pertussis, was shown to increase delayed-type hypersensitivity (DTH) to protein antigens in mice. First, it caused an approximately twofold enhancement of the magnitude of 24-h DTH reactions. Second, the peak magnitude of DTH was delayed to 4-7 d after challenge, at which time it was five times more intense than in mice not receiving pertussigen. This reaction was antigen specific, and histologically was characterized by a dense mononuclear infiltrate. Third, pertussigen prolonged DTH so that it was still detectable 3-6 wk after challenge. The effect of pertussigen was seen only in antigen-driven reactions and was time and dose dependent, with 400 ng given 3 d after immunization resulting in the most prolonged reaction. The administration of pertussigen to the recipients of sensitized lymph node cells resulted in DTH that was more intense and prolonged than the reactions in control mice. Administration of pertussigen provides a model of prolonged and enhanced T cell-dependent inflammatory responses.


2001 ◽  
Vol 8 (3-4) ◽  
pp. 193-200 ◽  
Author(s):  
Miodrag L. Lukic ◽  
Eric Mensah-Brown ◽  
Sehamuddin Galadari ◽  
Allen Shahin

Dark Agouti (DA) rats are highly susceptible to induction of Th-l-mediated autoimmunity disease, including experimental allergic encephalomyelitis (EAE). In contrast to other susceptible rat strains in which disease is induced only with encephalitogen emulsified in complete Freund's adjuvants (CFA), in DA rats EAE develops after injection of encephalitogen in incomplete Freund's adjuvants (IFA) or Titermax, putative Th-2 directed adjuvant. Lymph node cells derived from immunized DA rats and stimulatedinvitroproduce significantly more Interferon-γ(IFN-γ) than resistant Albino Oxford (AO) rats. However, cells derived from both strains produce large amounts of IL-10 but not IL-4. Immunized lymph node cells derived from EAE susceptible (AO × DA) F1rats induce clinical signs of disease in sublethally irradiated parental DA but not AO rats. The pathohistology of the target tissue in these recipients clearly demonstrated infiltration of mononuclear cells in both parental strains. However, the number of CD4+cells was significantly higher and number of apoptotic cells significantly lower in DA rats sacrificed 8 days after passive transfer. We postulate that in addition to higher IFN-γand TNF-α production, resistance to early apoptosis of the invading cells in the target tissue possibly due to lack of downregulation by TGF-β leads to exceptional susceptibility to EAE in DA rats.


2020 ◽  
Vol 48 ◽  
Author(s):  
Adjanna Karla Leite Araujo ◽  
Adriana Leão de Carvalho Lima Gondim

Background: Canine visceral leishmaniasis is a worldwide zoonosis, with dogs being the main urban reservoirs. It is caused by a protozoan of the genus Leishmania spp. and is transmitted to mammals through a vector belonging to the phlebotomines family. Its treatment aims to reduce the parasitic load preventing these animals from being transmitters. Immunotherapy has been shown to be efficient in stimulating the patient's immune response, improving the general condition and preventing recurrence. This report describes the case of a dog diagnosed with canine visceral leishmaniasis submitted to immunotherapy and drug protocol, noting significant general improvement.Case: An 8-year-old female dog was treated with ulcerated lesions on the paw pads, nasal plane and lip region, onychogryphosis and ungeitis, in addition, hypertrophied popliteal lymph nodes and erosive lesions in the elbows, without improvement with previous treatments. Serological examination was then performed to diagnose leishmaniasis by the immunosorbent assay (ELISA) technique with negative results.  In addition, was performed puncture of the popliteal lymph node, sample in which amastigote forms of Leishmania were observed and blood sample analysis by immunochromatographic rapid test showing reagent result, confirming the diagnosis of canine visceral leishmaniasis. The treatment protocol with marbofloxacin, allopurinol, prednisolone and domperidone was initiated. Thirty days later, there was a total improvement of the lesions and healing of the paw pads. Immunotherapy was then initiated by applying three double doses of recombinant vaccine against canine visceral leishmaniasis. The applications were made subcutaneously, with an interval of 21 days between them, still maintaining allopurinol. After six months a fourth double dose of the vaccine was applied and ten days later a new serological examination was performed using the Indirect Immunofluorescence Reaction (IIFR) technique with total dilution, with the result not reagent. Four months later, the patient was reevaluated and a new serological test was performed through the IIFR technique with total dilution and the result was reagent with high titration (1: 320). Then began the use of milteforan and domperidone. After two months, the patient received a new vaccination booster and the use of domperidone was discontinued. After ten days a new serological examination was performed using the IIIRF technique with total dilution, with reagent result, but with minimal titration (1:40).Discussion: Canine visceral leishmaniasis is a systemic zoonosis of major public health importance. The dog, due to its proximity to humans, is considered the main reservoir of the disease. Although clinical signs are nonspecific, skin lesions such as nasal hyperkeratosis, ulcers and hyperpigmentation, as well as clinical manifestations such as lymphadenopathy, fever, epistaxis and ophthalmic changes are frequently observed. In this case, the patient presented most of the lesions described in the literature. Laboratory abnormalities in blood count and serum biochemistry, commonly observed, were not observed in the animal. The ELISA serological test, despite being used as a screening test, due to its ability to detect low antibody titers, was negative in this case. The diagnosis was confirmed by lymph node cytology, described in the literature as a confirmatory test despite being considered invasive by most authors and positive result in rapid immunochromatography test. With the protocol used, the animal showed improvement, being observed negative results or with low titration of anti-leishmania antibodies in a serological test performed using the IFAT technique, indicating a decrease in parasitic load.


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