Decreased tuftsin concentrations in patients who have undergone splenectomy.

Spirer, Z; Zakuth, V.; Diamant, Shmuel; Mondorf, W.; Stefănescu, T; Stabinsky, Y.; Fridkin, Mati

doi:10.1136/bmj.2.6102.1574

Cited by 59 publications

(18 citation statements)

References 12 publications

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“…In contrast to the low values in elective removal of the spleen for therapeutic or staging purposes, splenectomy after accidental rupture of the spleen does not usually result in tuftsin deficiency [9,34,46,47]. Values obtained indicate that only the occasional case shows tow tuftsin serum values.…”

Section: Acquired Tuftsin Deficiencymentioning

confidence: 47%

“…This is based on a radioimmunoassay where nanogram quantities can be measured. Again, in tuftsin deficiency considerably lower levels than normals are obtained [46,47].…”

Section: Acquired Tuftsin Deficiencymentioning

confidence: 86%

“…Recently, with the use of the more accurate and quantitative radioimmunoassay by Spirer, Fridkin et al [18,46,47] it was possible to show that cases with elective splenectomy show values of about 120 ng/ml as compared with normals with about 255 ng/ml.…”

Section: Acquired Tuftsin Deficiencymentioning

confidence: 98%

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Klinische und physiologische aspekte von Tuftsin-Mangelsyndromen mit gest�rter Phagocytose

Najjar

1979

Klin Wochenschr

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The tetrapeptide tuftsin (Thr-Lys-Pro-Arg) stimulates phagocytosis by blood neutrophilic granulocytes and tissue macrophages in a highly specific manner. Tuftsin is cleaved off the carrier gamma-globulin molecule as the free active form by two enzymes. One of these is in the spleen and the other on the outer membrane of the phagocyte. Congenital tuftsin deficiency usually arises when the peptide is mutated to an inactive peptide. The acquired type occurs if the spleen function is curtailed by removal or disease. Tuftsin deficiency is manifested by severe recurrent infections involving primarily the skin, lymph nodes and lungs. Therapy is limited to gamma-globulin injection along with appropriate chemotherapy.

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Section: Acquired Tuftsin Deficiencymentioning

confidence: 47%

“…This is based on a radioimmunoassay where nanogram quantities can be measured. Again, in tuftsin deficiency considerably lower levels than normals are obtained [46,47].…”

Section: Acquired Tuftsin Deficiencymentioning

confidence: 86%

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Klinische und physiologische aspekte von Tuftsin-Mangelsyndromen mit gest�rter Phagocytose

Najjar

1979

Klin Wochenschr

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“…The other, which cleaves offthe carboxy end, is an enzyme which has not been properly characterized, yet seems to be located in the spleen. The very fact that splenectomized organisms are susceptible to bacterial infections was attributed to the decrease in tuftsin levels due to the lack of the spleen enzyme [7,[11][12][13]. Thus, the release of tuftsin from the Fc bound Ig seems to determine the capacity of the Ig to trigger phagocytosis, since it is the tetrapeptide, and not the intact Ig which signals the macrophages.…”

Section: Introductionmentioning

confidence: 99%

Immunostimulation by an Ig derived tetrapeptide, tuftsin

Tzehoval

Segal

Stabinsky

et al. 1979

Springer Semin Immunopathol

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Studies were carried out on the effects of a tetrapeptide tuftsin (Thr-Lys-Pro-Arg)l associated with the Ig heavy chain, to increase the capacity of antigen pulsed macrophages to 'educate' T-lymphocytes. We demonstrated that a simultaneous application of KLH and synthetic tuftsin to monolayers of macrophages, increased significantly the lymphoproliferative response of lymph node cells recruited by initiator T-cells which were generated in culture on the macrophage monolayers. Tuftsin coupled covalently at its C-terminal site to BSA increased antibody response to BSA. We compared the effects of various synthetic structural analogues of tuftsin on the activation of the immunogenic effects of the antigen presenting macrophage. These experiments indicated that tuftsin activates the immunogenic macrophages not by stimulating phagocytosis, i. e., not by increasing the uptake of antigen by the macrophages. Its effect seems to be controlled by the stero-specific properties of the tetrapeptide determined by the specific sequence of the amino acids. It appears, however, that the dominant entity for the stimulation of the immunogenic macrophage is the Pro-Arg sequence. Since quite a number of peptide-hormones seem to possess Pro-Arg or Arg-Pro sequences, this may indicate a general principle for the activation of the programmed state of cells.

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“…This molecule is a part of a specific carrier γG 1 cytophilic globulin which is cleaved by an enzyme through two steps, the first occurring in the spleen and the second on neutrophil granulocytes or monocytic-macrophagic cell membrane [2]. Tuftsin deficiency has been found in several diseases and is chiefly attributable to impaired splenic function [3,4,5,6,7,8,9]. Such a defect may participate to development of the increased susceptibility to bacterial infections of these conditions.…”

Section: Introductionmentioning

confidence: 99%

Effect of Liver Transplantation on Tuftsin Activity and Phagocytic Activity of Neutrophil Granulocytes in Patients with Liver Cirrhosis

Foschi

Trevisani

Loggi

et al. 2005

Int Arch Allergy Immunol

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Background: Tuftsin activity (TA) is reduced in cirrhosis. This contributes to the defective phagocytic activity (PA) of neutrophil granulocytes and is related to the impairment of splenic function. Orthotopic liver transplantation (OLT) cures cirrhosis and might restore TA. This study was aimed at determining if OLT restores TA and PA. Methods: We measured in 9 cirrhotic patients, before and after successful OLT, TA by a bioassay and PA by chemiluminescence in which neutrophils of the patient were tested with both autologous (PA1) and pooled sera from healthy subjects (PA2). Splenic function was assayed by the pitted red cell count. Results: Before OLT, TA was reduced in 7 patients, and PA1 in all the patients. Pitted cell count was elevated in all the patients. After OLT (median 39 months; range 21–49), TA improved in all cases [median: from 8% (5–16%) to 20% (9–22%), p < 0.008], normalizing in 5 out of the 7 patients with low values. PA1 improved in all the patients [from 102 cpm (65–128 cpm) to 235 cpm (78–280 cpm), p < 0.008], normalizing in 5. Pitted red count decreased in 7 patients and normalized in 3 [from 3.3% (2.1–6.0%) to 2.4% (1.4–2.8%), p < 0.021]. Platelet count [from 55 × 10³ (30–100) to 185 × 10³ (93–286), p < 0.008] and leucocyte count [from 3.60 × 10³ (1.81–5.23) to 5.53 × 10³ (3.31–6.71), p < 0.008] also improved. Conclusions: OLT improves TA and PA of cirrhotic patients. This effect is associated with an improvement of both functional hyposplenism and haematological hypersplenism. The restoration of natural defences against infections may mitigate the adverse effect of immunosuppressive treatment.

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Decreased tuftsin concentrations in patients who have undergone splenectomy.

Cited by 59 publications

References 12 publications

Klinische und physiologische aspekte von Tuftsin-Mangelsyndromen mit gest�rter Phagocytose

Klinische und physiologische aspekte von Tuftsin-Mangelsyndromen mit gest�rter Phagocytose

Immunostimulation by an Ig derived tetrapeptide, tuftsin

Effect of Liver Transplantation on Tuftsin Activity and Phagocytic Activity of Neutrophil Granulocytes in Patients with Liver Cirrhosis

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