Anti‐Pr<sub>3</sub>: Serological and Immunochemical Identification of a New Anti‐Pr Subspecificity

Roelcke, D.; Ébert, W.; Geisen, H. P.

doi:10.1111/j.1423-0410.1976.tb02802.x

Cited by 52 publications

(9 citation statements)

References 26 publications

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“…Other examples of auto-anti-M have been reported in the literature (Fletch and Zmijewski, 1970;Hysell et al, 1973;Tegoli et al, 1970) but the majority of cases did not show any similar clinical significance. Other blood group specificities have been implicated with cold-agglutinin disease; these are anti I, anti i (Issitt and Issitt, 1976), anti-Gd, and anti-Pr (Roelcke et al, 1976). These are rarely associated with cryoglobulins.…”

Section: Discussionmentioning

confidence: 99%

Anti blood group-M autoantibodies with livedo reticularis, Raynaud's phenomenon, and anaemia.

Sangster¹,

Kenwright²,

Walker³

et al. 1979

J Clin Pathol

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SUMMARY A 63-year-old woman presented with Raynaud's phenomenon and extensive cold-induced livedo reticularis. A skin biopsy showed no abnormality of the blood vessels but the blood contained high titres of a very unusual autoantibody against the M blood group, most active at low temperatures. An IgM cryoglobulin was detected, and anti-M activity was found in this fraction. Livedo reticularis may occur in a wide variety of diseases affecting the blood vessels of the skin or the theological properties of the blood (Champion, 1965;Copeman, 1975). We describe the case of a woman with Raynaud's phenomenon and severe and extensive livedo reticularis regularly induced by cold and abolished by warmth, in whom the only abnormality found was an unusual anti-M autoantibody most active at low temperatures. Case historyA 63-year-old housewife was admitted to The London Hospital in May 1977 complaining of purplish discoloration of the limbs. Ten months before admission she developed severe intermittent cramping pain in the upper arms, which was worse at night; this lasted for about three months and then resolved. At about the same time as the pain she noticed purple mottling especially of the hands but also of the arms and legs. This was worse in the cold and disappeared completely when she was very warm. For six months before admission she had noticed Raynaud's phenomenon affecting the hands. Prednisolone, 10 mg daily, had been given for some weeks without benefit. She had had tuberculosis of the spine and rheumatic fever as a girl. She had had two miscarriages, and two live births with healthy infants. She had never had a blood transfusion. For some years before admission INVESTIGATIONSHaemoglobin 9.5 g/dl, haematocrit 0-291, mean corpuscular volume 92 fl, mean corpuscular haemoglobin 30-3 pg, mean corpuscular haemoglobin concentration 32-4 g/dl. Anisocytosis, polychromasia, and agglutination of the red cells were noted, but unfortunately a reticulocyte count was not performed. The blood count was repeated three months later in warm weather and showed a haemoglobin of 12-8 g/dl and a reticulocyte count of 1-2 %. The white cells and platelets were normal. Serum total bilirubin 28 ,tmol/l (1 -6 mg/100 ml) direct 5 ,umol/l (0-3 mg/ 100 ml), liver function tests otherwise normal. A biopsy of affected skin showed no abnormality on histological or immunofluorescent examination; the blood vessels were normal. The following were also normal or negative: antinuclear factor and autoantibody screen, latex fixation test, plasma protein electrophoresis, serum iron, vitamin B12 and folate, red-cell folate, urea and electrolytes, Treponema pallidum, haemagglutination, and VDRL slide test, microscopy and culture of the urine, and x-rays of the chest, skull, and hands. X-ray of the lumbar 154 on 10 May 2018 by guest. Protected by copyright.

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Section: Discussionmentioning

confidence: 99%

Anti blood group-M autoantibodies with livedo reticularis, Raynaud's phenomenon, and anaemia.

Sangster¹,

Kenwright²,

Walker³

et al. 1979

J Clin Pathol

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“…Absorption and heat elution procedures of cold-type autoanti bodies with untreated human RBCs were performed following the method of Roelcke et al [12]. Serial dilutions of 0.1 ml of serum or heat eluate from RBCs were mixed with 0.05 ml of a 3% RBC suspension and incubated at 4°C for 2 h [9].…”

Section: Cold-type Autoantibody Testingmentioning

confidence: 99%

Characterization of Autoantibodies in Mixed-Type Autoimmune Hemolytic Anemia

Kajii¹,

Miura²,

Ikemoto³

1991

Vox Sanguinis

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Three of 46 patients with autoimmune hemolytic anemia (AIHA) satisfied the diagnostic criteria for mixed-type AIHA in which both warm-type and cold-type autoantibodies against red blood cells (RBCs) are present. The specificities of these autoantibodies were analyzed. All of the warm-type autoantibodies were IgG-x, and the specificities were not serologically classified. The autoantibody of patient 1 reacted to the 41- and 80-kD peptides on immunoblotting, and the epitope corresponding to it was papain sensitive. Two warm-type autoantibodies from patients 2 and 3 resembled each other in serological analyses and reacted with a protease- and neuraminidase-resistant antigen. However, the antigen corresponding to the autoantibody of patient 3 was located on the 37-kD peptide by immunoprecipitation. All of the cold-type autoantibodies were IgM-x and showed high titer and high thermal amplitude. According to the reaction pattern with untreated and enzyme-treated RBCs, the cold-type autoantibodies of patients 2 and 3 were revealed to be anti-Om and anti-I, respectively. In patient 1, the cold-type autoantibody was characterized as having high affinity for autologous RBCs, but its specificity was unclassified. The antigens corresponding to the cold-type autoantibodies were not located by immunoblotting and immunoprécipitation. These serological and immunochemical approaches to autoantibodies in mixed-type AIHA revealed that the warm and cold components recognized the different antigens.

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“…As N ‐acetylneuraminic acid is the major determinant of the Pr antigens, treatment of RBCs with sialidase also eliminates Pr reactivity [11]. Anti‐Pr CAs may be further subdivided by their reactivity with chemically modified N ‐acetylneuraminic acid (Pr 1 , Pr 2 and Pr 3 ) and their reactivity with human (h) or dog (d) RBCs (Pr h and Pr d antigens) [11,13,14]. A certain subspecificity, termed anti‐Pr M , is characterized by serological reactivity, anti‐Pr‐like, at low temperatures (4 °C) and anti‐M‐like behaviour at higher temperatures [15].…”

Section: Introductionmentioning

confidence: 99%

Restriction in the repertoire of the immunoglobulin light chain subgroup in pathological cold agglutinins with anti‐Pr specificity

et al. 2004

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Including data from the literature, the repertoire of the light-chain variable domain in pathological anti-Pr cold agglutinins exhibits a clear bias towards the use of the single germline gene-derived subgroup, Vkappa IV (eight of 17 or 47%). The association of Vkappa IV subgroup light chain-containing anti-Pr cold agglutinins with binding to alpha 2,3-, but not alpha 2,6-linked N-acetyneuraminic acid raises speculations about a possible role of subgroup-derived determinants in anti-Pr binding.

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Anti‐Pr₃: Serological and Immunochemical Identification of a New Anti‐Pr Subspecificity

Cited by 52 publications

References 26 publications

Anti blood group-M autoantibodies with livedo reticularis, Raynaud's phenomenon, and anaemia.

Anti blood group-M autoantibodies with livedo reticularis, Raynaud's phenomenon, and anaemia.

Characterization of Autoantibodies in Mixed-Type Autoimmune Hemolytic Anemia

Restriction in the repertoire of the immunoglobulin light chain subgroup in pathological cold agglutinins with anti‐Pr specificity

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Anti‐Pr3: Serological and Immunochemical Identification of a New Anti‐Pr Subspecificity

Cited by 52 publications

References 26 publications

Anti blood group-M autoantibodies with livedo reticularis, Raynaud's phenomenon, and anaemia.

Anti blood group-M autoantibodies with livedo reticularis, Raynaud's phenomenon, and anaemia.

Characterization of Autoantibodies in Mixed-Type Autoimmune Hemolytic Anemia

Restriction in the repertoire of the immunoglobulin light chain subgroup in pathological cold agglutinins with anti‐Pr specificity

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Anti‐Pr₃: Serological and Immunochemical Identification of a New Anti‐Pr Subspecificity