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Biomedical subjects

L H Perrin

Publications and source records attributed to L H Perrin.

At least 73 records · Page 4Linked to original sources
PubMed1980

Immunopathological aspects of Plasmodium berghei infection in five strains of mice. I. Immune complexes and other serological features during the infection.

The development of circulating immune complexes was studied in mice of the BALB/c, A/J, OF1, CBA and C57B1 strains infected with P. berghei. Complexes were evaluated in relation to levels of parasitaemia, soluble antigen, specific antibody and C3. Susceptibility to infection was greatest in BALB/c, A/J and OF/a mice. The maximum parasitaemia was 30% in CBA and 70% in all other strains. Levels of soluble antigen paralleled those of parasitaemia. Specific antibody was detected in all strains, but the titre continued to rise throughout the infection only in CBA mice. Circulating immune complexes occurred in mice of all strains from day 6; the level fell after day 9 in C57B1 whereas it was maintained in CBA mice. The development of immune complexes was associated with marked depression of C3 levels in all except CBA mice, in which a transient reduction was followed by recovery. Partial characterization of the complexes showed that IgM-containing complexes appeared earliest and reached highest levels in BALB/c mice while in CBA mice, IgM complexes were found in lesser amounts and the level fell in late infection. IgG complexes rose throughout infection in CBA and fell in later stages in BALB/c and C57B1 mice. In nude BALB/c mice, immune complexes were usually not detectable and only low levels of antibody of IgM class were produced. Differences in mortality pattern could not be related to any single serological factor.

Animals↗
PubMed1979

[Demonstration of soluble parasite antigens, the corresponding antibodies and immune complexes in acute malaria].

Serum levels of malaria antigens, antimalaria antibodies, immune complexes and complement components have been followed up in 23 patients suffering from acute malaria infection and recovering under therapy. Malarial antigens in serum were detected by counterimmunoelectrophoresis: the peak was observed before therapy started and their levels rapidly decreased. Specific antimalarial antibodies became detectable 5--7 days after starting treatment in patients with a first infection. Immune complexes were detected in 21 of 23 sera with a peak level between days 5 and 9. A marked decrease of C4 and C3 was observed in the presence of normal levels of factor B.

Antibodies↗
PubMed1979

Lysis of measles virus-infected cells by the purified cytolytic alternative complement pathway and antibody.

The dependence of antibody-and-complement-mediated lysis of virus-infected cells on the alternative pathway was examined utilizing the isolated cytolytic alternative pathway--a system consisting of the six purified proteins of the alternative pathway of activation (C3, factors B and D, beta 1H, C3b inactivator and properdin), and the five proteins of the membrane attack pathway (C5--9) of complement. HeLa cells acutely infected with measles virus were lysed by anti-viral IgG and the isolated cytolytic alternative pathway with an efficiency comparable to whole human serum. IgG and its F(ab')2 fragment were equally effective in inducing lysis by the isolated cytolytic alternative pathway, binding of approximately equal to 5 X 10(7) molecules per cell being required for 50% lysis; in contrast, no lysis occurred when equivalen or greater amounts of Fab' were bound to the virus-infected cell. Properdin was required for lysis. No lysis occurred if properdin was deleted from the isolated cytolytic alternative pathway, and lysis was diminished by 80% in properdin-depleted serum. Uptake of [125I]C3b from the isolated alternative pathway onto measles virus-infected cells occurred in the absence of properdin, but was accelerated in the presence of properdin. The 11 proteins of the isolated cytolytic alternative pathway are thus sufficient for lysis of measles virus-infected cells bearing anti-viral IgG or F(ab')2 without any other serum protein.

Antibodies, Viral↗
PubMed1979

Circulating and tissue-bound immune complex formation in murine malaria.

Immune complex formation during Plasmodium berghei infection of OF1 mice was investigated. Circulating immune complexes (CIC) were detected by the Clg-binding assay and the conglutinin-binding solid-phase assay in lethal or drug-limited infections. CIC appeared on day 9 of infection, peaked on day 11, and disappeared only after complete cure of the infection. Analysis of the immune complexes detected by the Clq-binding assay revealed the following characteristics: sedimentation coefficients of 13S to 21S, resistance to DNAse, and selective removal by filtration through protein A bound to Sepharose. Glomerular deposits of IgM preceded the appearance of CIC, whereas deposits of IgG and C3 were concomitant with the appearance of CIC. Tissue-bound immunoglobulins were also found in the choroid plexus. The appearance of anti-malarial antibodies and malarial antigens in the serum was closely associated with a depression of C3 levels and the presence of CIC. Drug treatment was followed by normalization of C3 levels, and clearance of both CIC and malarial antigens.

Animals↗
PubMed1978

[Specific cytolytic activity of human lymphocytes following vaccination with vaccinia virus and measles virus].

Human peripheral lymphocytes harvested 7 days after vaccination with vaccinia virus or measles virus lyse specifically target cells infected with the corresponding virus. This cytotoxic activity is found in a subpopulation of lymphocytes depleted of T-cells and containing lymphocytes bearing Fc receptor. The activity can also be transferred by supernatant of immune lymphocytes on addition of normal lymphocyte. These results suggest that two types of cell are involved: an antibody-secreting cell providing specific antiviral antibody (B-cells), and an effector cell bearing Fc receptor (K-cells).

Adult↗
PubMed1978

Generation of virus-specific cytolytic activity in human peripheral lymphocytes after vaccination with vaccinia virus and measles virus.

Human peripheral blood lymphocytes (PBL) harvested after vaccination with vaccinia or measles virus showed a specific activity against virus-infected target cells. This activity peaked on day 7 and was specific for the target cells infected with the virus used for the vaccination. The cytotoxic activity was not related to HLA markers. The cells involved in the cytolytic process were lymphocytes bearing Fc receptors. In addition, the cytotoxic activity was abrogated by more than 90% by rabbit Fab'2 anti-human IgG. It is therefore likely that two subpopulations of lymphocytes are involved: an antibody-secreting cell providing specific antiviral antibody and an effector cell bearing Fc receptor (K cells). Finally, these experiments suggest that antibody-dependent cell cytotoxicity may play a major role in the recovery from virus infection in man.

Adult↗
PubMed1977

Immune response in humans after vaccination with vaccinia virus: generation of a virus-specific cytotoxic activity by human peripheral lymphocytes.

After vaccinia virus vaccination of human volunteers, local indurations developed within 10 days, and regional adenopathy was detected in half of the individuals. Their peripheral blood lymphocytes (PBL) harvested at different days after vaccination showed specific activity against target cells infected with vaccinia virus with a peak activity at day 7. The specificity of the cytotoxic activity was not related to HLA markers, since autologous, homologous, and heterologous infected target cells were lysed with the same efficiency. The cytotoxic activity was caused by PBL that did not rosette with sheep erythrocytes and could be depleted by more than 90 percent by removing Fc receptor-bearing cells. T-cell- depleted PBL showed a one-half to two times greater cytotoxicity than intact PBL. The cytotoxic activity could also be abrogated by more than 95 percent by rabbit Fab(2) anti-human IgG. On the other hand, nonimmune PBL lysed vaccinia-infected target cells in the presence of specific antibodies against vaccinia virus, thus demonstrating that ADCC could be efficient in lysing vaccinia-infected target cells. We conclude that after vaccination, antibody-forming cells arise and provide specific anti-viral antibody and that the cytotoxic cells detected in this reaction are K cells. These experiments suggest that antibody-dependent cell cytotoxicity may be of major importance in the recovery of man to virus infections.

Adult↗
PubMed1977

Lysis of human cultured lymphoblastoid cells by cell-induced activation of the properdin pathway.

Human cultured lymphoblastoid cells incubated in normal human serum activate the properdin complement pathway without antibody. However, only cells bearing C3b immune adherence receptors bind components of the properdin complement pathway and undergo lysis. A similar surveillance mechanism may exist in man to limit growth of malignant B cells bearing C3b immune adherence receptors.

B-Lymphocytes↗
PubMed1977

Correlation between levels of breakdown products of C3, C4, and properdin factor B in synovial fluids from patients with rheumatoid arthritis.

Synovial fluids from 31 patients with seropositive rheumatoid arthritis (RA) and 23 patients with seronegative RA had significantly increased levels of breakdown products to C3, C4, and properdin factor B when compared to patients with osteoarthritis (OA) (P less than 0.01). The same patients exhibited a considerable overlap of native C3, C4, and properdin factor B levels when their results were compared with those of OA patients. The parallel increase of C3d, C4d, and Ba levels in patients with RA suggests an activation of the complement system rather than a nonspecific enzymatic breakdown in synovial fluids.

Arthritis, Rheumatoid↗
PubMed1977

Immunologic injury in measles virus infection. III. Presence and characterization of human cytotoxic lymphocytes.

Human peripheral blood leukocytes (PBL) from patients with chronic measles virus infection (SSPE) or from immune, adult humans (convalescent from acute childhood measles virus infection) are cytotoxic for target cells infected with measles virus as measured by a 51Cr assay. Specific release of 51Cr by immune PBL occurred both with and without human antibodies added to measles virus-infected cultures. Maximal killing in the absence of added antibodies to measles virus was usually detected only after 15 to 18 hr of incubation and with a high PBL to target ratio (100:1). When antibody to measles virus was added, PBL-mediated killing of virus-infected cells was not blocked. Instead, killing was enhanced and maximal lysis occurred with fewer PBL and a shorter incubation time. This cytotoxic reaction was inhibited in a dose-response manner upon the addition of Fab fragments of IgG containing antibodies to measles virus. On the average 4 to 5 x 105 antibody molecules bound per infected target cell before initiation of antibody-enhanced PBL killing. Depletion of either glass-adhering or E-rosette-forming cells did not reduce PBL killing of measles virus-infected target cells in either system. In contrast, removal of non-E rosette or of EAC rosette-forming population of PBL almost completely abrogated cytotoxicity. When Fc-bearing cells were removed, killing of virus-infected target cells was concomitantly reduced. Lysis of measles virus-infected target cells did not require histocompatibility between the PBL and the target cell. Further, immunospecific lymphocyte killing was not enhanced by such a histocompatibility fit. These experiments indicate first, that the effector PBL involved in lysis of measles virus-infected targets are not T cells but are probably K cells and, second, that PBL obtained from patients with SSPE are competent in killing measles virus-infected targets. Moreover, sera from SSPE patients did not contain a factor(s) that blocked PBL-mediated cytotoxicity.

Antibodies, Viral↗
PubMed1977

The formation and fate of virus antigen-antibody complexes.

We report the fate of 125I human IgG measles virus antibodies complexed to virus antigens expressed on the surfaces of HeLa cells persistently infected with measles virus. Each HeLa cell expressing viral antigens on its surface bound about 7.5 x 106 IgG molecules under saturation conditions. Three hours after 125I antiviral IgG bound to and saturated all antigenic sites on infected cells, 30% of the counts were released (85% TCA ppt), after 12 hr 60%, and after 24 hr 75% (30% TCA ppt). By linear sucrose density centrifugation about 30% of the counts released from infected cells at 3 hr sedimented faster than 7S IgG, 60% sedimented at the 7S position whereas 10% (non-TCA ppt) were found at the top of the gradient. Using specific rabbit antibody to measles virus hamagglutinin or nucleocapsid, we found that hemagglutinin, but not nucleocapsid antigen, was present in the heavy complexes. These experiments show that after anti-measles virus antibody binds to cell surface measles viral antigens (i.e.. hemagglutinin), immune complexes form and are shed into culture fluids. In addition part of immune complex is endocytosed and broken into small m.w. components. Shedding of virus antigen-antibody complexes from the cell's surface may be an important source of the circulating complexes found in virus-infected humans and animals.

Antibodies, Viral↗
PubMed1976

Evidence for immune-complex formation in patients with amyotrophic lateral sclerosis.

Immune complexes have been found in several chronic diseases of unknown aetiology and identification of the constituents of the complexes might lead to recognition of aetiological agents. Sera and renal tissues from patients with amyotrophic lateral sclerosis (A.L.S.) were studied for evidence of immune complexes. C1q precipitation testing demonstrated that sera from 10 of 25 patients with classic A.L.S. bound significantly more radiolabelled C1q than sera from 15 controls. In renal glomeruli studied for deposition of host 1gG, C3, fibrinogen, and albumin by means of direct immunofluorescence, 9 of 33 patients with A.L.S. (27 biopsy and 6 necropsy specimens) had moderate amounts of both IgG and C3 of granular basement membrane and mesangia. This pattern of immunofluorescence is characteristic of immune complex deposits. Of these 9, 8 had rapidly progressive neurological courses, whereas among the remaining 18 patients with no evidence of immune-complex disease, 9 of 12 available for clinical follow-up had stable or slowly progressive courses.

Amyotrophic Lateral Sclerosis↗
PubMed1976

Mechanism of injury of virus-infected cells by antiviral antibody and complement: participation of IgG, F(ab')2, and the alternative complement pathway.

Antibody-mediated C-dependent lysis of cell lines infected with herpes simplex type 1 virus, influenza A degrees virus, measles virus, and mumps virus occurred by the alternative C pathway with the participation of IgG antibodies. Lysis occurred only with immune human sera, Mg++ EGTA immune sera, and immune sera depleted of C4 or treated with Fab anti-C4. Lysis did not occur with nonimmune sera, Mg++ EDTA immune sera, and immune sera heated 50 degrees C for 25 min, depleted of factor B or treated with Fab antifactor B. Lysis was restored to heated and factor B immunodepleted immune sera by addition of factor B, but not by addition of an excess of C2. Further studies showed that lysis of HeLa cells infected with measles virus was induced by both immune IgG and F(ab')2 but not Fab' in the presence of a nonantibody-containing human C source. Lysis of measles virus-infected cells was also indpendent of movement of viral antigens on the surface of the infected cells, as inhibition of viral antigen capping by cytochalasin B or sodium azide was not associated with abrogation of immune lysis.

Antibodies, Viral↗
PubMed1976

Binding of components of the properdin system to cultured human lymphoblastoid cells and B lymphocytes.

Immunofluorescence studies showed that properdin (P) and factor B bind to C3-C3b receptor bearing human lymphoblastoid cells (Raji, Daudi) and B type human peripheral lymphocytes (HPL). P bound to Raji cells first incubated with normal human serum (NHS). EDTA, but not EGTA, halted the binding of P to cells incubated with NHS. However, fixation of P to Raji cells, after incubation with NHS first reacted with inulin, was independent of Ca++ and -g++ ions. Fixation of P to Raji cells depended on the presence of C3 or C3b and occurred in the absence of factor D and factor B. Binding of P to B type HPL was detectable only after incubation of these cells with NHS first reacted with inulin; under these conditions binding of P to Raji cells was also greatly enhanced. With both Raji cells and HPL, factor B was detectable on cell surfaces only after incubation of these cells with NHS first reacted with activators of the P system. Binding of factor B to cells required the presence of C3b and binding or stabilization of cell bound factor B necessitated the presence of activated P. P and factor B were detectable only on cultured cells having C3-C3b receptors. However, incubation of NHS with all lymphoblastoid cell lines studied resulted in activation of P and cleavage of factor B. Binding of P and factor B to cells may follow one of three sequences; (a) activated P in fluid phase combines with C3, factor D, and factor B, and the whole complex fixes to cellular C3-C3b receptors via its C3 moiety; (b) C3b generated in fluid phase combines with P, C3, factor D, and factor B and binds to C3-C3b receptors; or (c) C3 or C3b first binds onto the C3-C3b receptors and thereafter interacts with P, factor D, And factor B. Binding of components of the P system to cells or other particles may relate to such biological phenomena as lysis, phagocytosis, proliferation, attraction of other cell types, and alteration of responsiveness to external stimuli.

ABO Blood-Group System↗