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Biomedical subjects

G B Mackaness

Publications and source records attributed to G B Mackaness.

At least 37 records · Page 2Linked to original sources
PubMed1974

Influence of dose and route of antigen injection on the immunological induction of T cells.

Delayed-type hypersensitivity (DTH) develops in the absence of an adjuvant when mice are injected intravenously or subcutaneously with an appropriate dose of sheep red blood cells (SRBC). The optimal intravenous dose of 10(5) SRBC (in CD-1 mice) produces maximum DTH which decays exponentially from its peak on day 4. Increasing the dose of SRBC reduces and eventually abolishes all evidence of DTH. DTH fails to reappear in respose to secondary stimulation except in splenectomized mice in whom the development of DTH is not suppressed, even by massive doses of SRBC. Hence the suppression cannot be due to antigen as such. The optimal dose of SRBC for sensitization by footpad inoculation is 100-fold higher (10(7) SRBC in CD-1 mice), but even 10(9) SRBC do not block the induction of DTH by this route of immunization. A blocking dose of SRBC, given intravenously 1 day before footpad inoculation, completely suppresses cell proliferation in the draining lymph node, prevents PFC production there, and blocks the induction of DTH by a sensitizing dose of SRBC. If given 1 day after footpad sensitization, intravenous antigen has little effect on the cellular response in the regional node but DTH is still completely suppressed. Blocking of induction and expression may depend, therefore, on different mechanisms.

Animals↗
PubMed1974

Feedback inhibition of specifically sensitized lymphocytes.

An explanation was sought for the fact that delayed-type hypersensitivity (DTH) does not normally occur in response to T-cell-dependent antigens unless an adjuvant is used. But when sheep red blood cells (SRBC) were administered intravenously DTH did appear, provided that the dose of antigen was less than that required to give a maximum antibody response. Animals in which T-cell activity had been blocked by a large dose of antigen could not be sensitized adoptively, and their spleen cells failed to transfer DTH to normal recipients. The serum of blocked animals partially inhibited the induction of DTH, and after absorption with SRBC its blocking activity increased substantially. Moreover, absorbed serum inhibited DTH in previously sensitized animals, but it did not inhibit the proliferative response to SRBC in peripheral lymph nodes or reduce the number of plaque-forming cells produced therein. On the contrary, the hemagglutinating titer was actually increased by blocking serum even though DTH was totally suppressed. It is concluded that a product of the interaction between antigens and antibody blocks the activated T cells which mediate DTH without interfering with helper cells.

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↗
PubMed1973

Immune response to Mycobacterium tuberculosis in rats.

After intravenous injection into rats, both the attenuated strain R1Rv and the virulent strain H37Rv of Mycobacterium tuberculosis grow in the liver and spleen. However, the infected rats mount a specific immune response with great rapidity, giving a false impression of natural resistance to the tubercle bacillus. Adoptive immunity to tuberculosis was achieved by transferring thoracic duct cells from immunized donors to normal syngeneic recipients. The transferred immunity was vested in a population of lymphocytes uncontaminated with macrophages. The adoptive immunity was effectively expressed against both attenuated and virulent tubercle bacilli, and it was shown to be immunologically specific. Lymphocytes which conferred immunity to tuberculosis were not protective against Listeria monocytogenes infection, and vice versa. Immunity could not be transferred with either normal thoracic duct lymphocytes (TDL), heat-killed sensitized TDL, or serum from specifically immunized donors. The ability of TDL from BCG-immunized donors to confer immunity was maintained at an unimpaired level for at least 3 months after immunization.

Animals↗
PubMed1971

The mediator of cellular immunity. I. The life-span and circulation dynamics of the immunologically committed lymphocyte.

Thoracic duct cells from rats which have survived an infection with Listeria monocytogenes can confer a high level of antimicrobial resistance upon normal recipients. The cells which confer protection appear in the thoracic duct during the 1st wk of the immunizing infection, at a time when newly formed lymphocytes are being added to the lymph in substantially increased numbers. The protective cells differ in at least two respects from the majority of small lymphocytes in central lymph: they have a rapid turnover rate and a short life-span in the circulation. Evidence was also obtained that lymphopoiesis affecting the long-lived small lymphocyte, which belongs to the recirculating pool, is not increased during an acute Listeria infection.

Animals↗
PubMed1971

The mediator of cellular immunity. II. Migration of immunologically committed lymphocytes into inflammatory exudates.

Peritoneal exudates from rats which have survived an infection with L. monocytogenes can protect cyclophosphamide-treated recipients against a Listeria challenge. They are more effective in this respect than cells obtained from the spleen or thoracic duct lymph. Since exudate cells from normal rats and inocula prepared from the resident peritoneal cell populations of infected donors are unable to inhibit the challenge infection, the protective cells must belong to a class of lymphocytes that emerges from the blood in response to inflammation. It is significant therefore that thoracic duct lymphocytes formed during an acute Listeria infection can move into exudates induced by a variety of inflammatory stimuli. The affinity of newly formed lymphocytes for inflamed tissue points to a mechanism whereby the host marshalls its cellular defenses at sites of bacterial invasion. The tendency of short-lived lymphocytes to leave inflamed vessels might also explain their short-circulating life-span.

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