Lymph node accessory cells in the immune response

1984 ◽  
Vol 237 (1) ◽  
pp. 39-42 ◽  
Author(s):  
E. W. A. Kamperdijk ◽  
M. van den Berg ◽  
E. C. M. Hoefsmit
Keyword(s):  
Immune Response ◽  
Lymph Node ◽  
Accessory Cells

New developments in drugs enhancing the immune response: activation of lymphocytes and accessory cells by muramyl-dipeptides

1979 ◽  
pp. 133-160 ◽  
Author(s):  
R. H. Gisler ◽  
F. M. Dietrich ◽  
G. Baschang ◽  
A. Brownbill ◽  
G. Schumann ◽  
...  
Keyword(s):  
Immune Response ◽  
New Developments ◽  
Accessory Cells ◽  
Response Activation

scholarly journals MACROPHAGE-LYMPHOCYTE CLUSTERS IN THE IMMUNE RESPONSE TO SOLUBLE PROTEIN ANTIGEN IN VITRO

1974 ◽  
Vol 140 (5) ◽  
pp. 1245-1259 ◽  
Author(s):  
Ole Werdelin ◽  
Otto Brændstrup ◽  
Eskild Pedersen
Keyword(s):  
Immune Response ◽  
Lymph Node ◽  
Cluster Formation ◽  
Peritoneal Macrophages ◽  
Physical Interaction ◽  
Antigen Binding ◽  
Purified Protein Derivative ◽  
Cell Clusters ◽  
Immune Lymphocytes

We have studied the physical interaction between macrophages and lymphocytes during the immune response to purified protein derivative of tuberculin (PPD) in vitro. Mixtures of peritoneal macrophages and lymph node lymphocytes from guinea pigs immunized with tubercle bacilli formed cell clusters during 20 h of culture with PPD. The number of clusters produced was correlated to the number of immune lymphocytes in the cultures. Peritoneal macrophages which had been pulsed with PPD and untreated lymph node lymphocytes produced cell clusters in the absence of free PPD in numbers equivalent to those produced by the same cells in the presence of free PPD. In cultures containing a mixture of PPD-pulsed macrophages, not-pulsed macrophages, and immune lymphocytes with no free PPD, cell clusters developed mainly between the antigen-pulsed macrophages and lymphocytes. Cluster formation was antigen-specific with the specificity residing in the lymphocytes, mainly or exclusively in the T lymphocytes. These data indicate that in the process of cell cluster formation macrophages serve as antigen-binding (or -processing) cells, while a subpopulation of lymphocytes interact physically and specifically with the macrophages.

Abstract 454: Evaluating the progression of cutaneous melanoma by the molecular immune response of the sentinel lymph node

2015 ◽  
Author(s):  
Richard Essner ◽  
Alexandra Gangi ◽  
David Kaufman ◽  
Ke Wei Gong ◽  
Myung Sim ◽  
...  
Keyword(s):  
Immune Response ◽  
Lymph Node ◽  
Sentinel Lymph Node ◽  
Cutaneous Melanoma

scholarly journals MATURATION OF THE IMMUNE RESPONSE IN VITRO

1972 ◽  
Vol 136 (2) ◽  
pp. 353-368 ◽  
Author(s):  
Alberto J. L. Macario ◽  
Everly Conway de Macario ◽  
Claudio Franceschi ◽  
Franco Celada
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Lymph Node ◽  
Association Constant ◽  
Secondary Response ◽  
Antibody Specificity ◽  
Affinity Selection ◽  
Immune Response In Vitro ◽  
Selection Of

We have cultivated lymph node microfragments from ß-D-galactosidase (Escherichia coli) primed rabbits and have measured their secondary response directed towards the whole molecule (precipitating antibodies) and to a single determinant (activating antibodies) of the antigen. By decreasing the size of the fragments to 105 cells, we began to observe heterogeneity among identical cultures in terms of positivity of response, antibody specificity, and titers. The affinity of "early" activating antibodies was inversely proportional to the dose of challenge. While no maturation was seen in low and excessive challenge, in all cultures receiving intermediate doses the association constant was raised several orders of magnitude within periods of 20 days. The relevance of these data to the mechanism of affinity selection of antigen-sensitive cells is discussed.

scholarly journals Regulation of lymph node vascular growth by dendritic cells

2006 ◽  
Vol 203 (8) ◽  
pp. 1903-1913 ◽  
Author(s):  
Brian Webster ◽  
Eric H. Ekland ◽  
Lucila M. Agle ◽  
Susan Chyou ◽  
Regina Ruggieri ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Proliferation ◽  
Endothelial Cells ◽  
Dendritic Cells ◽  
Lymph Node ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Cell Trafficking ◽  
Vascular Growth ◽  
Draining Lymph Node

Lymph nodes grow rapidly and robustly at the initiation of an immune response, and this growth is accompanied by growth of the blood vessels. Although the vessels are critical for supplying nutrients and for controlling cell trafficking, the regulation of lymph node vascular growth is not well understood. We show that lymph node endothelial cells begin to proliferate within 2 d of immunization and undergo a corresponding expansion in cell numbers. Endothelial cell proliferation is dependent on CD11c+ dendritic cells (DCs), and the subcutaneous injection of DCs is sufficient to trigger endothelial cell proliferation and growth. Lymph node endothelial cell proliferation is dependent on vascular endothelial growth factor (VEGF), and DCs are associated with increased lymph node VEGF levels. DC-induced endothelial cell proliferation and increased VEGF levels are mediated by DC-induced recruitment of blood-borne cells. Vascular growth in the draining lymph node includes the growth of high endothelial venule endothelial cells and is functionally associated with increased cell entry into the lymph node. Collectively, our results suggest a scenario whereby endothelial cell expansion in the draining lymph node is induced by DCs as part of a program that optimizes the microenvironment for the ensuing immune response.

scholarly journals THE IMMUNE RESPONSE TO SHEEP ERYTHROCYTES IN THE MOUSE

1967 ◽  
Vol 126 (1) ◽  
pp. 15-33 ◽  
Author(s):  
David Eidinger ◽  
Hugh F. Pross
Keyword(s):  
Immune Response ◽  
Lymph Node ◽  
Latent Period ◽  
Lymphoid Cells ◽  
Secondary Response ◽  
Lymphoid Tissues ◽  
Antibody Activity ◽  
Cellular Activity ◽  
Sheep Erythrocytes ◽  
Draining Lymph Node

The direct and indirect plaque technique for the detection of antibody-forming cells against sheep erythrocytes was utilized for the investigation of a number of biological parameters of the primary and secondary immune response on a cellular level. The sequential pattern of 19S followed by 7S antibody formation was elicited in the primary response after a latent period of at least 1–2 days and 2–3 days respectively. The secondary response initiated 140 days after primary immunization, in contrast, was characterized by the simultaneous appearance of 19S and 7S antibody-forming cells after an observed latent period of 2–3 days. The cellular dynamics of the recruitment phase of the respective immunoglobulins in the primary and secondary response was interpreted as evidence for the derivation of the two classes of immunoglobulins from separate progenitors. The 19S antibody-forming cells were derived predominantly by a process of transformation and maturation and 7S antibody formers by a process of cellular division with a doubling time of about 12 hr. The draining lymph node exhibited maximal immunological reactivity due to its capacity to retain the particulate antigen. This capacity was considerably enhanced in the sensitized draining lymph node. Minimal cellular activity was also noted in distal lymphoid tissues which included the thymus. Focal cellular activity was observed in the draining lymph node for 60 days after immunization. Subsequently, very low level plaque-forming cellular activity was observed in association with persistence of maximal antibody activity. The appearance at 120 days of a generalized peak of cellular activity in lymphoid tissues throughout the host was considered an explanation for this discrepancy. The change in distribution of cellular antibody-forming activity, from a local to a generalized lymphatic response during the late phase of the immune response, implied a fundamental alteration in homeostatic mechanisms associated with maintenance of immune reactivity. Further manifestations of such an alteration were indicated by the appearance of 2-ME-sensitive 7S antibody nearly 3 months after primary intradermal immunization, which in the ensuing 5 months was associated with, and inversely related to, two major fluctuations in 2-ME-resistant 7S antibody. Evidence for the existence of immunological memory in the 19S system was not established in the present work. 19S anamnesis, for which evidence was derived from measurements of circulating antibody levels, was interpreted from cellular studies as the result of the substantial activity of previously uncommitted 19S lymphoid cells in distal lymphoid tissue associated with previously committed 19S cells contained in the draining lymph node.

scholarly journals INDUCTION AND REVERSAL OF IMMUNE PARALYSIS IN VITRO

1970 ◽  
Vol 132 (5) ◽  
pp. 845-857 ◽  
Author(s):  
V. S. Byers ◽  
E. E. Sercarz
Keyword(s):  
Immune Response ◽  
Cell Proliferation ◽  
Lymph Node ◽  
Cell Population ◽  
Antibody Production ◽  
Cellular Environment ◽  
Immune Paralysis ◽  
Antigen Removal ◽  
The Postponement

Induction of the immune response can only be completed after antigen is removed from the cellular environment. Primed rabbit lymph node fragments were cultured in vitro with 5 mg/ml BSA. If antigen was removed from the fragments 2 hr later, they produced a normal anti-BSA response, which was first evident 5 days later. If antigen removal was delayed for 3 days, the onset of the response was postponed for 2 to 3 days. Pulses with BUDR marked the periods of cell proliferation in both sets of cultures, and established that the postponement of antibody production was preceded by a postponement in the wave of proliferation among precursors of antibody forming cells. The similarity in avidity of antibody-containing fluids from normal and postponed cultures support the idea that the same cell population produced the response in each case. It was concluded that a reversible state of paralysis could be instituted in antigen-responsive cells, and this state did not depend upon cell-killing. The widespread incidence of temporary paralysis as an early aspect of the immune response was discussed.

scholarly journals Initiation of the adaptive immune response to Mycobacterium tuberculosis depends on antigen production in the local lymph node, not the lungs

2007 ◽  
Vol 205 (1) ◽  
pp. 105-115 ◽  
Author(s):  
Andrea J. Wolf ◽  
Ludovic Desvignes ◽  
Beth Linas ◽  
Niaz Banaiee ◽  
Toshiki Tamura ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
Lymph Node ◽  
T Cell Activation ◽  
Cd4 T Cells ◽  
Adaptive Immune Response ◽  
Adaptive Immune ◽  
Initial Activation ◽  
Local Lymph Node

The onset of the adaptive immune response to Mycobacterium tuberculosis is delayed compared with that of other infections or immunization, and allows the bacterial population in the lungs to expand markedly during the preimmune phase of infection. We used adoptive transfer of M. tuberculosis Ag85B-specific CD4+ T cells to determine that the delayed adaptive response is caused by a delay in initial activation of CD4+ T cells, which occurs earliest in the local lung-draining mediastinal lymph node. We also found that initial activation of Ag85B-specific T cells depends on production of antigen by bacteria in the lymph node, despite the presence of 100-fold more bacteria in the lungs. Although dendritic cells have been found to transport M. tuberculosis from the lungs to the local lymph node, airway administration of LPS did not accelerate transport of bacteria to the lymph node and did not accelerate activation of Ag85B-specific T cells. These results indicate that delayed initial activation of CD4+ T cells in tuberculosis is caused by the presence of the bacteria in a compartment that cannot be mobilized from the lungs to the lymph node, where initial T cell activation occurs.

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