Der selektive Nachweis von HLA-spezifischen B-Gedächtniszellen

2021 ◽  
Vol 11 (04) ◽  
pp. 245-250
Author(s):  
Gwendolin Simper ◽  
Philipp Schleumann ◽  
Sarah Seidel ◽  
Gia-Gia Toni Ho ◽  
Susann Placzko ◽  
...  
Keyword(s):  
Hla Antigen

ZusammenfassungIn der Transplantationsdiagnostik werden die Seren der Patienten auf der Warteliste jedes Quartal auf präexistierende Anti-HLA-Antikörper untersucht. Jedoch kann die Existenz von zirkulierenden peripheren Antikörpern, die von knochenmarkresidierenden Plasmazellen sezerniert wurden, keine zuverlässige Information über das Zellkompartment von B-Gedächtniszellen geben. Die Exposition mit einem inkompatiblen HLA-Antigen kann immer die Aktivierung vorhandener B-Gedächtniszellen auslösen. Die Analyse von B-Gedächtniszellen ermöglicht die Erhebung von belastbaren Daten über den individuellen Immunstatus eines Patienten.

The Mechanism of Platelet Aggregation Induced by HLA-Related Antibodies

1996 ◽  
Vol 76 (05) ◽  
pp. 774-779 ◽  
Author(s):  
John T Brandt ◽  
Carmen J Julius ◽  
Jeanne M Osborne ◽  
Clark L Anderson
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Complement Activation ◽  
Thromboembolic Disease ◽  
Clinical Samples ◽  
Hla Antigen ◽  
Aggregation Response ◽  
Immune Mediated ◽  
Dependent Pathway

SummaryImmune-mediated platelet activation is emerging as an important pathogenic mechanism of thrombosis. In vitro studies have suggested two distinct pathways for immune-mediated platelet activation; one involving clustering of platelet FcyRIIa, the other involving platelet-associated complement activation. HLA-related antibodies have been shown to cause platelet aggregation, but the mechanism has not been clarified. We evaluated the mechanism of platelet aggregation induced by HLA-related antibodies from nine patients. Antibody to platelet FcyRIIa failed to block platelet aggregation with 8/9 samples, indicating that engagement of platelet FcyRIIa is not necessary for the platelet aggregation induced by HLA-related antibodies. In contrast, platelet aggregation was blocked by antibodies to human C8 (5/7) or C9 (7/7). F(ab’)2 fragments of patient IgG failed to induce platelet activation although they bound to HLA antigen on platelets. Intact patient IgG failed to aggregate washed platelets unless aged serum was added. The activating IgG could be adsorbed by incubation with lymphocytes and eluted from the lymphocytes. These results indicate that complement activation is involved in the aggregation response to HLA-related antibodies. This is the first demonstration of complement-mediated platelet aggregation by clinical samples. Five of the patients developed thrombocytopenia in relationship to blood transfusion and two patients developed acute thromboembolic disease, suggesting that these antibodies and the complement-dependent pathway of platelet aggregation may be of clinical significance.

HLA antigen frequencies and Wegener's granulomatosis

2009 ◽  
Vol 16 (5) ◽  
pp. 448-451
Author(s):  
G.E. MURTY ◽  
B.T. MAINS ◽  
D. MIDDLETON ◽  
A.P. MAXWELL ◽  
D.A. SAVAGE
Keyword(s):  
Wegener’S Granulomatosis ◽  
Wegener's Granulomatosis ◽  
Hla Antigen

scholarly journals Epidemiology and Pathogenesis of Nasal NK/T-Cell Lymphoma: A Mini-Review

2011 ◽  
Vol 11 ◽  
pp. 422-428 ◽  
Author(s):  
Katsuyuki Aozasa ◽  
Mona A. A. Zaki
Keyword(s):  
T Cell ◽  
Latin American ◽  
Cell Lymphoma ◽  
Gene Mutations ◽  
T Cell Lymphoma ◽  
Upper Respiratory Tract ◽  
Case Control Studies ◽  
Hla Antigen ◽  
Barr Virus ◽  
Nk T Cell

Nasal NK/T-cell lymphoma (NKTCL) frequently presents with necrotic, granulomatous lesions in the upper respiratory tract, and usually shows a highly aggressive clinical course. Thus, it was initially included in the clinical condition of lethal midline granuloma. Recently, the disease has been recognized as a neoplastic proliferation of NK/T cells. The disease is much more frequent in Asian and Latin American countries than in Western countries, and is universally associated with Epstein-Barr virus (EBV) infection. Analyses of gene mutations, especially p53 and c-kit, revealed the different frequencies by district. Abnormalities of other genes have also been reported. Case-control studies showed that the exposure to pesticides and chemical solvents could be causative of NKTCL. Further studies including HLA antigen typing of patients is necessary to further clarify the disease mechanism.

scholarly journals Identification of platelet proteins that bind alloantibodies and autoantibodies

Blood ◽  
1984 ◽  
Vol 64 (6) ◽  
pp. 1240-1245 ◽  
Author(s):  
DV Devine ◽  
WF Rosse
Keyword(s):  
Membrane Proteins ◽  
Western Blot ◽  
Hla Antigens ◽  
Cell Types ◽  
Igg Antibody ◽  
Hla Antigen ◽  
Molecular Weights ◽  
Plasma Factors ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract We have used the techniques of radioimmunoprecipitation (RIP) and Western blot to identify the membrane proteins that bind certain alloantibodies. Anti-PlA1 sera precipitated two bands, corresponding to platelet glycoproteins IIb and III, whether or not calcium was present during the procedure. By Western blot, this antibody bound only glycoprotein III. Anti-PlA1 serum does not precipitate proteins from the platelets of a patient with Glanzmann's thrombasthenia. Two monoclonal antibodies reacting with lymphocyte HLA antigens, as well as sera from highly allosensitized patients, precipitated bands of 38,500 and 13,500 daltons. These bands correspond to the molecular weights of the two subunits of the HLA antigen, as it has been described for other cell types. The patients' sera also precipitated a protein of 72,000 daltons from some platelets. The sera of two patients with quinidine- induced thrombocytopenia precipitated a 138,000-dalton band (glycoprotein Ib-alpha) in the presence of quinidine. The purified IgG antibody from one patient did not require other plasma factors to bind to platelets in the presence of quinidine, while purified antibody from a second patient required plasma factors other than, or in addition to von Willebrand factor. Although several sera from patients with idiopathic thrombocytopenic purpura (ITP) were tested, only one precipitated membrane proteins by the RIP method; this serum identified binding proteins corresponding to glycoproteins IIb and III.

scholarly journals Effect of leukocyte antibodies and HLA matching on the intravascular recovery, survival, and tissue localization of 111-indium granulocytes

Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 522-528 ◽  
Author(s):  
J McCullough ◽  
M Clay ◽  
D Hurd ◽  
K Richards ◽  
C Ludvigsen ◽  
...  
Keyword(s):  
Hla Antigens ◽  
Pulmonary Sequestration ◽  
Strong Relationship ◽  
Immunofluorescence Assay ◽  
Hla Matching ◽  
Hla Antigen ◽  
Tissue Localization ◽  
The Relationship

The effect of leukocyte antibodies detected under different conditions on the fate in vivo of granulocytes was studied using 111-indium- labeled granulocytes. Sera from patients were tested by granulocyte agglutination (GA), granulocytotoxicity (GC), granulocyte immunofluorescence (GIF), lymphocytotoxicity (LC), and antibody- dependent lymphocyte-mediated granulocytotoxicity. Granulocytes from donors to be studied were labeled with 111-indium and injected. Then the intravascular recovery and survival or tissue localization was determined in 93 studies. Antibodies detected by granulocyte agglutination were associated with a significant reduction in recovery (6.7% v 30.8% in controls; P less than .001) and t1/2 (0.3 hours v 5.6 hours in controls; P = .002). When all possible combinations of serum reactivity were considered, reactivity in the GA plus GIF assays had the best correlation with decreased recovery (R2 = .49; P less than .001) and t1/2 (R2 = .73; P less than .001). When the relationship between the strength of antibody reactivity and the recovery and t1/2 were analyzed, the best relationship was between the combination of LC and GIF with recovery (R2 = .62; P = .001). Because of the general availability of the HLA (LC) testing, the role of LC reactivity was investigated in other ways. There was a strong relationship between sera highly reactive by LC and those reactive by GIF. These highly reactive sera were also associated with reduced recovery and t1/2. The influence of specific HLA antigen mismatches was also studied. When donor and recipient were mismatched for the HLA-A2, B8, or BW44 antigens, there was a significant reduction in either recovery, t1/2, or both. Tissue localization was studied by body scans in patients with and without known sites of inflammation. Antibodies detected by a combination of GA and GIF caused abnormal pulmonary sequestration of granulocytes (three cases) and failure of granulocytes to localize at known sites of inflammation (three cases). HLA (LC) antibodies did not alter tissue localization despite the presence of the corresponding HLA antigens on granulocytes. It appears that GA, GIF, or a combination of these tests is the most effective predictor of altered in vivo fate of granulocytes. However, sera highly reactive by LC and GIF probably define a group of highly immunized patients in whom granulocyte recovery and t1/2 are also reduced. Mismatching for certain HLA antigens is also associated with reduced granulocyte recovery and survival. At present, GA, with or without the immunofluorescence assay, is the most effective predictor of altered in vivo granulocyte activity.(ABSTRACT TRUNCATED AT 400 WORDS)

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