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R J North

Publications and source records attributed to R J North.

At least 127 records · Page 7Linked to original sources
PubMed1975

Mchanisms of antitumor action of Corynebacterium parvum: nonspecific tumor cell destruction at site of immunologically mediated sensitivity reaction to C. parvum.

Mice immunized in the footpad with Corynebacterium parvum developed a systemic mechanism with a potential for destroying syngeneic tumor cells. The development of this mechanism of antitumor action depended on the generation of a state of systemic sensitivity to C. parvum antigens, which allowed an immunologically mediated inflammatory response to be focused at the site of a tumor cell challenge or in the bed of an established tumor. This resulted in complete inhibition of growth of the former regression of the latter. This nonspecific mechanism of tumor cell destruction could be utilized only during a relatively short period when mice were responding maximally to the organism. This corresponded to a period during which there was maximum cell division in the lymph node draining the site of immunization with C. parvum, maximum systemic macrophage activation, and maximum sensitivity to eliciting injections of the organism. The potential for destroying tumor cells could be transferred to normal recipients with lymph node cells from C. parvum-immunized donors, which indicated the distinct possibility that antitumor action was based on the cell-mediated response to C. parvum antigens. That the destruction of tumor cells at the site of a C. parvum sensitivity reaction was associated with a massive influx of mono-nuclear cells provided further support for this possibility.

Animals↗
PubMed1975

Nature of "memory" in T-cell-mediated antibacterial immunity: anamnestic production of mediator T cells.

Mice that survived an immunizing infection with Listeria monocytogenes remained specifically resistant to lethal secondary infection for several months. This acquired, long-lived state of resistance was not dependent on activated macrophages that remained after the primary response. It depended, instead, on an acquired long-lived capacity on the part of immunized mice for generating mediator T cells faster and in larger numbers than normal mice. The number of mediator T cells generated in response to secondary infection was proportional to the level of infection. The results suggest that the accelerated production of mediator T cells that occurs in response to secondary infection represents the expression of a state of immunological T-cell memory.

Animals↗
PubMed1975

Nature of "memory" in T-cell mediated antibacterial immunity: cellular parameters that distinguish between the active immune response and a state of "memory".

Immunizing infection in mice with Listeria monocytogenes resulted in the generation of two distinct states of immunological reactivity. There was generated (i) a short-lived state of active immunity that functioned to urgently eliminate the infection organism from the tissues and (ii) a long-lives state of increased immunological potential that enabled the host to respond to seconday infection in an accelerated manner. Short-lived active immunity was mediated by replicating T cells and expressed by activated macrophages, and it ended when these cell types disappeared from the tissue soon after complete elimination of the parasite. Long-lived immunological protential was associated with a persistent level of delayed sensitivity and with the presence of a small number of nonreplicating protective T cells. It is suggested that the state of delayed sensitivity represents a state of immunological T-cell memory of the cell-mediated type.

Animals↗
PubMed1974

T cell dependence of macrophage activation and mobilization during infection with Mycobacterium tuberculosis.

Mice made T cell-deficient as adults by thymectomy and lethal irradiation, and infected with Mycobacterium tuberculosis, showed a greatly reduced capacity to develop nonspecific resistance to challenge with a heterologous bacterium. The capacity to develop nonspecific resistance was restored, however, by an infusion of syngeneic thymocytes. Evidence was presented which showed that the capacity of mycobacteria-infected mice to resist a lethal challenge with a heterologous organism rested on the capacity of macrophages existing at the time of challenge to reduce the number of challenge organisms to a sublethal level within 8 h. This antibacterial activity of macrophages was substantially reduced in T cell-deficient mice but could be restored by an infusion of syngeneic thymocytes. It was concluded that T cell-deficient mice have a reduced capacity to mobilize and activate macrophages because of their reduced capacity to respond immunologically to antigens of M. tuberculosis.

Animals↗
PubMed1974

Inflammatory lymphocyte in cell-mediated antibacterial immunity: factors governing the accumulation of mediator T cells in peritoneal exudates.

The lymphocytes which mediate immunity to infection with Listeria monocytogenes in the mouse accumulated in casein-induced peritoneal exudates. They were T cells, as evidenced by their susceptibility to anti-theta serum, but some were also destroyed by anti-immunoglobulin serum. For a given number of cells, exudate cells were at least six times more efficient than spleen cells in protecting normal recipients against lethal challenge. The extent to which mediator cells accumulated in exudates was found to be governed by the level of their production in responding lymphoid tissue and by the time available for them to migrate into an exudate. An intraperitoneal injection of casein at any stage of infection resulted in a progressive accumulation of mediator cells that continued for 3 days. The accumulation was not caused by continuous entry of cells during the whole of this period, but resulted from division of a limited number of cells that entered during the first 24 h. Accumulation of mediator cells in an exudate was associated with the conversion of a population of dividing cells into a population of nondividing T cells with a relatively short life-span.

Animals↗
PubMed1973

Cellular mediators of anti-Listeria immunity as an enlarged population of short lived, replicating T cells. Kinetics of their production.

An intravenous immunizing infection with the facultative, intracellular parasite, Listeria monocytogenes results in the production in the spleen of a population of immunologically-committed lymphocytes which can adoptively immunize normal recipients against a lethal challenge infection. These cellular mediators of immunity are first produced in the spleen between days 2 and 4 of infection and reach peak production on day 6. Their production then progressively decreases until about day 20 when their presence can no longer be detected. Increased production of cellular mediators is coincident with major increases in cell division, cellularity, and spleen weight. Decreased production of cellular mediators, on the other hand, is associated with decreases in cell division, cellularity, and spleen weight. Again, the level of delayed sensitivity to Listeria antigens expressed by the host at any one time is proportional to the number of cellular mediators in the spleen. Increased production of cellular mediators is also associated with major increases in the total numbers of replicating T cells and B cells in the spleen. That the cellular mediators of immunity are part of the replicating T cell population, rather than the B cell population, is evidenced by their susceptibility to anti-theta serum and by their resistance to anti-Ig serum. Furthermore, they can be completely eliminated from the spleen by a brief pulse of the antimitotic drug, vinblastine. This study allows the conclusion that the cellular mediators of anti-Listeria immunity belong to an expanded population of rapidly dividing, short-lived T cells. It is suggested that they have the same properties as the T cell effectors of allograft immunity.

Animals↗
PubMed1973

Immunological control of macrophage proliferation in vivo.

The transfer of cell-mediated anti-Listeria immunity to normal recipient mice with spleen cells from convalescing donors results in a striking increase in the replication of macrophages in the recipients' livers. Macrophage division occurs 24 h earlier and is 2 to 3 times more intense than macrophage division in mice combating infection with the aid of normal spleen cells. The spleen cells responsible for triggering increased macrophage division and for mediating immunity are destroyed by anti-theta serum and complement, thus showing that they are thymus derived lymphocytes. Their capacity to trigger macrophage division is not realized in the absence of an adequate number of replicating Listeria in the recipients' tissues.

Animals↗
PubMed1971

The action of cortisone acetate on cell-mediated immunity to infection. Suppression of host cell proliferation and alteration of cellular composition of infective foci.

Pulse labeling with tritiated thymidine shows that the response in the mouse to infection with L. monocytogenes includes a large increase in the division of lymphoid cells in the spleen, an increase in the division of macrophages in the liver, and an accumulation of monocyte-derived macrophages at infective foci in the tissues. A single 2.5 mg dose of cortisone acetate given at the beginning of infection greatly delays and suppresses these three components of the host response. The unrestricted bacterial multiplication which follows cortisone treatment is ultimately because of a failure of monocyte-derived macrophages to accumulate at infective foci where they normally express immunity. The accumulation of polymorphs at these sites, in contrast, is enhanced. It is argued that cortisone acetate prevents the accumulation of monocytes at infective foci indirectly by suppressing the production in the spleen of immunologically-committed lymphocytes which are needed to mediate the cellular events at infective foci.

Animals↗
PubMed1970

The relative importance of blood monocytes and fixed macrophages to the expression of cell-mediated immunity to infection.

Infection in mice with Listeria monocytogenes results in a substantial accumulation of migrant macrophages in the liver. The immigrant cells populate both the infective foci and intervening sinusoids. They have the labeling characteristics of blood monocytes, and their appearance in infective foci in the liver corresponds to the expression of a high level of antimicrobial immunity in this organ. The infected liver acquires additional new macrophages by Kupffer-cell division. The proliferation of these cells, however, is not essential for the expression of immunity in the liver. The results indicate that the macrophages which express immunity to a primary infection with L. monocytogenes are those derived from circulating monocytes. Most of these cells are quickly lost once the parasite is eliminated from the tissues.

Animals↗
PubMed1970

Suppression of cell-mediated immunity to infection by an antimitotic drug. Further evidence that migrant macrophages express immunity.

The development of acquired cell-mediated immunity to infection with Listeria monocytogenes can be blocked by a 15 hr pulse of the antimitotic drug, vinblastine (Vb). The drug has no effect on the host-parasite relationship after 72 hr of infection when a high level of immunity is being expressed, i.e., when infective foci are populated by activated macrophages. Infective foci in mice treated early during infection with Vb do not acquire migrant macrophages, but they become acellular after 48 hr of infection. The results indicate that Vb destroys the dividing precursors of migrant macrophages. The possibility that Vb prevents the activation of these cells by destroying dividing lymphoid cells engaged in the specific immunological phase of the host response is also considered.

Animals↗
PubMed1970

Endocytosis.

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Adenosine Triphosphate↗
PubMed1969

Cellular kinetics associated with the development of acquired cellular resistance.

Mice infected with either BCG or Listeria monocytogenes display the same type of cellular response pattern. In both infections there is an intense proliferation of splenic lymphoid cells, a coincident proliferation of differentiated macrophages, and a subsequent production of macrophages with increased metabolic potential. The temporal relations between these events and the onset of host resistance indicate that lymphoid cell proliferation and macrophage proliferation are essential events in the response which leads to cellular resistance against facultative intracellular parasites.

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