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M J Bogman

Publications and source records attributed to M J Bogman.

At least 55 records · Page 3Linked to original sources
PubMed1986

Expression of donor class I major histocompatibility antigens on the vascular endothelium of mouse skin allografts.

The expression of a class I MHC antigen on the vascular endothelium of mouse skin allografts was assessed by in vivo uptake of radiolabeled monoclonal anti-class-I antibody in the grafts after i.v. injection into the recipients. Endothelial localization of the bound antibodies was demonstrated via double-labeling immunofluorescence microscopy using factor-VIII-related antigen as a marker for endothelial cells. Treatment of recipients with cyclosporine was accompanied by low levels of class I antigen expression in the grafts, and similarly low levels were measured in grafts carried by nude recipients in the complete absence of rejection. Withdrawal of immunosuppressive therapy was followed by an increased class I antigen expression in the donor skin. An increase was also observed in skin grafts undergoing first-set rejection. We conclude that the expression of class I antigens on the capillary endothelium of mouse skin allografts in vivo is variable and is under influence of the immune status of the recipient.

Animals↗
PubMed1985

The spleen in Hodgkin disease: diagnostic value of CT.

Findings of CT of the spleen were compared with those of histologic examination in 35 patients who had Hodgkin disease. CT provides a simple way to calculate splenic size. This index is also of value in the assessment of the histologic state of the spleen. An accuracy rate of 91%, specificity of 94%, and a sensitivity of 89% in diagnosing splenic localization of lymphoma was found in this study.

Adolescent↗
PubMed1984

A comparative study of total body irradiation as a method of inducing granulocyte depletion in mice.

Since conventional methods of inducing depletion of polymorphonuclear granulocytes (PMNs) in mice, such as treatment with cytostatic drugs and anti-PMN sera, proved to be insufficient to induce a stable PMN depletion for several days, and were accompanied by considerable toxic side effects, we induced neutrophil depletion in mice by total body irradiation (TBI) in a single dose of 6.0 Gy (600 rads.) at a dose rate of 0.20 Gy/min. This treatment reduced the number of PMNs in the peripheral circulation to values below 150/microliter from day 3-10 after irradiation. The number of lymphocytes fell simultaneously. Platelet counts remained above 60% of normal values during the first 7 days after irradiation. Complement levels were not significantly affected by TBI. The results show that TBI of 6.0 Gy induces pronounced and stable PMN depletion in mice for at least 7 days. Furthermore, under an aseptic regimen the mice can be kept in good condition and losses are less than 5%.

Animals↗
PubMed1984

Combined immunodeficiency preceding chronic lymphocytic leukemia.

A 66-year-old female, suffering from recurrent infections of the respiratory tract, developed a severe hypogammaglobulinemia and an impaired cell mediated immunity in combination with abdominal lymphadenopathy and splenomegaly. Considering a lymphoid malignancy, an explorative laparotomy was performed. No malignancy could be established. After a follow-up of 2 years a diagnosis of chronic lymphocytic leukemia could be made. The onset of hypogammaglobulinemia 2 years before the development of chronic lymphocytic leukemia is not yet reported in the literature.

Agammaglobulinemia↗
PubMed1984

Absence of requirement for polymorphonuclear granulocytes in the acute antibody-mediated rejection of murine skin allografts.

The role of polymorphonuclear granulocytes (PMN) in acute antibody-mediated rejection (AAR) was studied in a murine skin allograft model. B10.A skin was grafted onto B10.D2 recipients that were treated with goat antimouse lymphocyte serum, to postpone cellular rejection. This prolonged the median survival time of the grafts to 21.5 +/- 1.0 days. PMN depletion was effected by total body irradiation of 6.0 Gy (600 rads) on day 4 after grafting, which reduced the number of PMN in the circulation to levels below 150/microliters from days 3-10 after the irradiation. To induce AAR the mice received, on day 8 after grafting, an i.v. injection of a monoclonal antibody with specificity against the donor H-2Kk antigen together with 0.25 ml fresh rabbit serum. This caused acute rejection of all grafts in the control group within 72 hr, with abundant presence of PMN in the graft vessels on histologic examination. In PMN-depleted recipients the reaction in the grafts was somewhat retarded in th first 24 hr, but nevertheless acute rejection occurred within 72 hr in 9 of 11 animals, whereas PMN were virtually absent from the grafts. The results show that PMN act as accelerators and amplifiers of the acute antibody-mediated rejection process, but are not essential mediators in the damage to the vascular endothelium of the grafts.

Animals↗
PubMed1984

Acute antibody-mediated rejection of skin grafts without involvement of granulocytes or complement.

In immunosuppressed mice that carry rat skin xeno-grafts, acute antibody-mediated graft rejection (AAR) can be induced by intravenous administration of mouse anti-rat globulin. Dependent on the amount of antibody injected and on the complement status of the recipient, an Arthus-like or a Shwartzman-like pattern of vasculitis occurs. The role of polymorphonuclear granulocytes (PMNs) in either type of vasculitis was tested by inducing AAR in recipients depleted of PMNs by total body irradiation. Despite the absence of PMNs in the graft vessels, AAR occurred both in the Arthus-like and in the Shwartzman-like type. Moreover, AAR could be elicited in PMN-depleted recipients that were complement-depleted by cobra venom factor treatment or were congenitally C5-deficient. We conclude that neither the PMN nor complement is an essential mediator the PMN nor complement is an essential mediator in this form of antibody-mediated vasculitis.

Agranulocytosis↗
PubMed1982

The role of complement in the induction of acute antibody-mediated vasculitis of rat skin grafts in the mouse.

Rat skin grafts carried by immunosuppressed mice can be acutely destroyed by intravenous administration of mouse anti-rat antibody. The velocity of the reaction and the histologic sequence of events depend on the amount of antibody administered: low doses give an Arthus-like rejection, whereas at high doses a Shwartzman-like pattern occurs. Depletion of C3 by cobra venom factor treatment did not prevent acute rejection after intravenous injection of high doses of antiserum but changed the reaction from a Shwartzman-like to an Arthus-like pattern. Conversely, supplementary administration of rabbit complement caused a violent Shwartzman-like graft destruction after injection of low doses of antibody, which in complement-normal mice gave an Arthus-like reaction. The results show that complement can greatly amplify the antibody-mediated immune vasculitis and can substantially modify its histologic pattern. It is, however, not an absolute requirement for the occurrence of the destructive process.

Acute Disease↗
PubMed1981

Complement-dependent and independent mechanisms in acute antibody-mediated rejection of skin xenografts in the mouse.

Complement dependency of acute antibody-mediated rejection (AAR) was studied in a xenogeneic skin graft model in the mouse. PVG/c rat skin grafted to immunosuppressed mice was acutely destroyed by i.v. administered mouse anti-rat serum on day 7 after grafting. Depression of the hemolytic complement titer in the recipients was indicative for complement consumption during the rejection process. Complete and long-lasting complement depletion induced by treatment with cobra venom factor (COVF) decreased the sensitivity of the grafts to AAR. However, complete protection was not achieved, since high doses of antidonor serum again induced destruction. Similar results were obtained in C5-deficient recipients and in COVF-treated C5-deficient recipients. These results indicated that complement-independent rejection mechanisms were operative. This was further substantiated by the finding that purified noncomplement-fixing IgC1 subclass antibodies were able to elicit mice with a normal complement status was caused by intravascular coagulation without primary involvement of polymorphonuclear leukocytes. In complement-depleted animals an Arthus-like reaction was seen, with dense intravascular accumulation of polymorphonuclear leukocytes (PMNs) that, apparently, were attracted to the graft through complement-independent mechanisms.

Animals↗
PubMed1980

Patterns of vascular damage in the antibody-mediated rejection of skin xenografts in the mouse.

Established rat skin grafts carried by immunosuppressed mice were acutely destroyed by an intravenous administration of mouse antirat lymphocyte serum. The histologic pattern of destruction was dependent on the amount of antiserum administered. At low doses (0.01 ml) an Arthus-like reaction was seen with early accumulation of granulocytes. At high doses (0.25 ml) a Shwartzman-like pattern occurred, with early intravascular thrombosis and without evident participation of granulocytes in the initial phases. Groups of mice that received intermediate doses showed graft changes that were transitional between these two types of destruction. Similar histologic patterns have been described in clinical transplantation. Our results show that they are not fundamentally different and that the severity of the triggering reaction determines which of either type will occur.

Animals↗
PubMedDate not supplied

Variable expression of Ia antigens on the vascular endothelium of mouse skin allografts.

Ia antigens are membrane-bound glycoproteins that play a part in antigen recognition and subsequent cell-cell interactions in the immune response. In the mouse they are coded for by the I region of the major histocompatibility complex H-2 and have been demonstrated on B lymphocytes, monocytes, activated T cells, macrophages and dendritic cells, including Langerhans cells. Ia-like antigens have also been detected on the vascular endothelium in man and on epidermal keratinocytes in rats but expression on the latter cells was induced by a graft-versus-host reaction or by contact hypersensitivity. In the mouse, previous studies have suggested that Ia antigens in skin are restricted to epidermal Langerhans cells and it was thought that these were the targets for Ia-dependent rejection of skin allografts. The results presented here show that Ia antigens in mouse allografts are also present on the vascular endothelium but their expression is variable and dependent on the immunological status of the recipient. These findings suggest that vascular endothelial cells can act as targets in Ia-incompatible skin allograft rejection.

Animals↗
PubMedDate not supplied

The spleen in non-Hodgkin lymphoma. Diagnostic value of computed tomography.

Computed tomography of the spleen was correlated with histologic examination or clinical data in 53 selected patients with non-Hodgkin lymphoma. Calculation of the splenic index with CT by multiplying spleen length, width and thickness is a simple and rapid procedure for defining splenic size in vivo. A good correlation was found between size of the spleen, as estimated by splenic index calculation, and the proven or probable histologic state of the spleen.

Adult↗