Passive immunity in rats infected withAngiostrongylus cantonensis: Interactions between syngeneic immune serum and sensitized lymph node cells

1982 ◽  
Vol 68 (1) ◽  
pp. 87-92 ◽  
Author(s):  
W. K. Yong ◽  
C. Dobson
Keyword(s):  
Lymph Node ◽  
Immune Serum ◽  
Passive Immunity ◽  
Lymph Node Cells

Interaction of Alveolar Macrophages with Nocardia asteroides : Immunological Enhancement of Phagocytosis, Phagosome-Lysosome Fusion, and Microbicidal Activity

1980 ◽  
Vol 30 (2) ◽  
pp. 578-587
Author(s):  
Carole Davis-Scibienski ◽  
Blaine L. Beaman
Keyword(s):  
Lymph Node ◽  
Alveolar Macrophages ◽  
Cell Damage ◽  
Immune Serum ◽  
Nocardia Asteroides ◽  
Bacterial Cells ◽  
Activated Macrophages ◽  
Additional Increase ◽  
Lining Material ◽  
Lymph Node Cells

Normal and specifically activated rabbit alveolar macrophages were infected in vitro with Nocardia asteroides GUH-2. In the presence of serum from normal rabbits, no significant differences were noted between normal and activated alveolar macrophages with respect to phagocytosis, incidence of phagosomelysosome fusion, or nocardicidal activity. However, all of these macrophage functions were enhanced by various immunological components. Serum from immunized rabbits enhanced phagocytosis of nocardial cells by activated macrophages, and there was an additional increase in phagocytosis observed when alveolar lining material was present. Complement had no effect on the ability of the macrophages to phagocytize nocardial cells. The greatest percentage of organisms phagocytized was observed when specifically primed lymph node cells, alveolar lining material, and serum from immunized rabbits were present in the incubation medium. N. asteroides GUH-2 inhibited phagosome-lysosome fusion in normal macrophages in the presence of serum from normal rabbits. However, addition of serum from immunized rabbits or the addition of specifically primed lymphocytes increased the amount of phagosome-lysosome fusion, whereas complement had no effect on this fusion process. Nocardial viability was not reduced when either normal or activated macrophages were infected with bacteria in the presence of normal serum, immune serum, or alveolar lining material. However, specifically activated macrophages incubated with primed lymph node cells obtained from immunized rabbits were able to both decrease the number of viable organisms recovered and to increase the incidence and extent of bacterial cell damage. The greatest number of organisms were killed by specifically activated macrophages when the bacterial cells were incubated with primed lymph node cells suspended in immune serum and alveolar lining material. These results indicate that activated macrophages alone are not sufficient to kill ingested N. asteroides GUH-2 and that specifically primed lymphocytes are important in host resistance to nocardial infections.

Immune expulsion of Trichuris muris from mice during a primary infection: analysis of the components involved

Parasitology ◽  
1975 ◽  
Vol 70 (3) ◽  
pp. 397-405 ◽  
Author(s):  
D. Wakelin
Keyword(s):  
Lymph Node ◽  
Mesenteric Lymph Node ◽  
Primary Infection ◽  
Immune Serum ◽  
Trichuris Muris ◽  
Mesenteric Lymph ◽  
Serum Transfer ◽  
Lymph Node Cells ◽  
Worm Expulsion ◽  
Sublethal Irradiation

Immune serum accelerated the expulsion of Trichuris muris when transferred into normal mice on days 0 and 3 after infection, but had no effect when the recipient mice had been immunosuppressed by sublethal irradiation or by cortisone treatment. Delaying serum transfer until days 7 and 8 in normal mice failed to accelerate expulsion, although immune mesenteric lymph node cells (MLNC) accelerated expulsion whether transferred early or late in infection.Expulsion from NIH mice, normally complete by 12 days, was prevented by sublethal irradiation given as late as 9 days after infection, but could be restored by subsequent transfer of immune MLNC or, to a lesser degree, non-immune MLNC. Immune MLNC were unable to restore worm expulsion in mice irradiated before infection.These results are interpreted as showing that the immune expulsion of T. muris from mice during a primary infection requires the sequential activities of antibody-mediated and lymphoid cell-mediated components.

A role for granulomatous inflammation in the transmission of infectious disease: schistosomiasis and tuberculosis

Parasitology ◽  
1997 ◽  
Vol 115 (7) ◽  
pp. 113-125 ◽  
Author(s):  
M. J. DOENHOFF
Keyword(s):  
Lymph Node ◽  
Immune Cell ◽  
Bacterial Pathogen ◽  
Granulomatous Inflammation ◽  
Immune Serum ◽  
Lung Pathology ◽  
A Cell ◽  
Lymph Node Cells ◽  
Excretion Rates ◽  
The Relationship

The relationship between cell-mediated granulomatous inflammation and transmission of disease in schistosomiasis and tuberculosis has been explored. In 2 experiments involving Schistosoma mansoni-infected normal and T cell-deprived mice, and infected deprived mice that had been variously reconstituted with immune or normal lymphocytes or immune serum, there was a significant positive numerical correlation between mean liver granuloma diameters and faecal egg counts in individual animals. Lymphocytes from donors with recently patent infections were more active than cells from chronically infected or uninfected donors in reconstituting egg excretion rates in deprived recipients, and mesenteric lymph node (MLN) cells were more active than spleen cells. Modulation of granulomatous activity with increasing chronicity of infection in the donors, resulting in a decrease in granuloma size around freshly produced tissue-bound eggs, was paralleled by a waning of the capacity of transferred lymph node cells to reconstitute egg excretion in the recipients. Serum taken from chronically infected donor mice over the same period and transferred to infected deprived recipients became more active in enhancing egg excretion in the recipients as the cell-mediated activity declined. A recent study in Kenya has found that S. mansoni-infected patients with concurrent human immunodefficiency virus (HIV) infection excrete fewer eggs than patients exposed to the same levels of schistosome infection, but who are not HIV-infected, thus indicating that schistosome egg excretion in humans is also immune-dependent. Attention is drawn to an apparently parallel situation in human tuberculosis, another pathogen which induces a cell-mediated granulomatous immune response. Several studies have shown that patients with tuberculosis who are also HIV-seropositive tend to have fewer tubercle bacilli detectable in their saliva than those with tuberculosis, but who are HIV-negative. This discrepancy, associated with differences in lung pathology in HIV-positive patients, suggests that in tuberculosis immune cell-mediated granulomatous inflammation causes the destruction of host tissue in a manner which facilitates onward transmission of the bacterial pathogen.

scholarly journals SPECIFICITY OF THE INFLAMMATORY RESPONSE IN VIRAL ENCEPHALITIS

1972 ◽  
Vol 136 (2) ◽  
pp. 216-226 ◽  
Author(s):  
Henry F. McFarland ◽  
Diane E. Griffin ◽  
Richard T. Johnson
Keyword(s):  
Bone Marrow ◽  
Lymph Node ◽  
Inflammatory Response ◽  
Sindbis Virus ◽  
Bone Marrow Cells ◽  
Immune Serum ◽  
Inflammatory Reactions ◽  
Virus Content ◽  
Lymph Node Cells ◽  
Marrow Cells

The viral-induced perivascular inflammatory response in Sindbis virus encephalitis of mice was shown to be immunologically specific. Mice were inoculated intracerebrally with Sindbis virus, and 24 hr later a single dose of cyclophosphamide was given which ablated the inflammatory response. 3 days after virus inoculation, cells and/or sera from specifically and nonspecifically sensitized donor mice were given, and the inflammatory reactions, virus content, and antibody response of recipients were examined 5 days later. Reconstitution of the viral inflammatory response required virus-specific sensitized lymph node cells and was enhanced when these lymph node cells were combined with bone marrow cells. Reconstitution was not achieved with Sindbis virus immune serum even when combined with nonspecifically sensitized cells. Combination of immune serum with Sindbis virus-sensitized cells did not produce an accentuation of the reaction. In distinction, reconstitution of the inflammatory reaction surrounding the stab wound was reconstituted with bone marrow cells from mice inoculated with Sindbis virus or control antigens. Reconstitution of the perivascular reaction was associated with a reduction in brain virus content. Although the transfer of Sindbis virus-sensitized lymph node cells and bone marrow cells resulted in the limited production of neutralizing antibody in the immunosuppressed recipient, the reduction in virus was significantly greater with the transfers of Sindbis virus-sensitized lymph node cells than with the passive transfer of immune serum alone.

scholarly journals The Distribution and Utilization of Glucose in Isolated Lymph Node Cells

1959 ◽  
Vol 234 (8) ◽  
pp. 1958-1965 ◽  
Author(s):  
Ernst Helmreich ◽  
Herman N. Eisen
Keyword(s):  
Lymph Node ◽  
Lymph Node Cells

scholarly journals Synthesis and Secretion of γ-Globulin by Lymph Node Cells

1967 ◽  
Vol 242 (13) ◽  
pp. 3242-3244
Author(s):  
Robert M. Swenson ◽  
Milton Kern
Keyword(s):  
Lymph Node ◽  
Lymph Node Cells

scholarly journals Screening and development of monoclonal antibodies for identification of ferret T follicular helper cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wenbo Jiang ◽  
Julius Wong ◽  
Hyon-Xhi Tan ◽  
Hannah G. Kelly ◽  
Paul G. Whitney ◽  
...  
Keyword(s):  
Animal Model ◽  
Monoclonal Antibodies ◽  
Lymph Node ◽  
Cross Reactivity ◽  
Tfh Cells ◽  
Follicular Helper ◽  
Lymph Node Cells ◽  
Human Viruses ◽  
Humoral Responses ◽  
Murine Monoclonal Antibodies

AbstractThe ferret is a key animal model for investigating the pathogenicity and transmissibility of important human viruses, and for the pre‐clinical assessment of vaccines. However, relatively little is known about the ferret immune system, due in part to a paucity of ferret‐reactive reagents. In particular, T follicular helper (Tfh) cells are critical in the generation of effective humoral responses in humans, mice and other animal models but to date it has not been possible to identify Tfh in ferrets. Here, we describe the screening and development of ferret-reactive BCL6, CXCR5 and PD-1 monoclonal antibodies. We found two commercial anti-BCL6 antibodies (clone K112-91 and clone IG191E/A8) had cross-reactivity with lymph node cells from influenza-infected ferrets. We next developed two murine monoclonal antibodies against ferret CXCR5 (clone feX5-C05) and PD-1 (clone fePD-CL1) using a single B cell PCR-based method. We were able to clearly identify Tfh cells in lymph nodes from influenza infected ferrets using these antibodies. The development of ferret Tfh marker antibodies and the identification of ferret Tfh cells will assist the evaluation of vaccine-induced Tfh responses in the ferret model and the design of novel vaccines against the infection of influenza and other viruses, including SARS-CoV2.

scholarly journals Transfer of experimental allergic encephalomyelitis in Lewis rats using supernates of incubated sensitized lymph node cells.

1977 ◽  
Vol 145 (5) ◽  
pp. 1405-1410 ◽  
Author(s):  
C C Whitacre ◽  
P Y Paterson
Keyword(s):  
Spinal Cord ◽  
Lymph Node ◽  
Guinea Pig ◽  
Experimental Allergic Encephalomyelitis ◽  
Nervous Tissue ◽  
Allergic Encephalomyelitis ◽  
Lewis Rats ◽  
Transfer Activity ◽  
Lymph Node Cells ◽  
Experimental Allergic

Supernates derived from incubated lymph node cells of Lewis rats sensitized to guinea pig spinal cord-Freund's adjuvant transfer experimental allergic encephalomyelitis (EAE) to syngeneic recipients. EAE supernatant transfer activity (EAE-STA) is not demonstrable in supernates derived from LNC of control donors not sensitized to nervous tissue. After addition of brain antigen to active supernates, EAE-STA is not longer demonstrable.

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