Cellular Resistance to Infection

Abstract

Antibody can influence the fate of bacteria in vivo by lysis or opsonisation. The former mechanism is of unknown significance. Opsonins, however, are important whenever the parasite can resist ingestion but is susceptible to inactivation within the phagocytes. Some organisms, however, can multiply within cells. The antibody response to such organisms is often at variance with the degree of resistance developed against them (1, 2). This has been taken as evidence for the existence of an alternative, non-humoral form of acquired resistance. It is widely held that the alternative mechanism is mediated by cells; but this view has not been wholly acceptable (2, 3), and the immunological basis for it has never been explained. Tuberculosis and brucellosis are two infections in which a cellular component has been claimed to play a role in acquired resistance, but they are ill-suited to an experimental approach to the problem. For one thing the immune state is not particularly efficient in either of them. But this is perhaps of less importance than the technical problems encountered in working with the tubercle bacillus, and the fact that virulent strains of Brucella are susceptible both to opsonisation (4) and to lysis by complement in the presence of specific antibody (5). Unless antibody can be excluded as a factor in acquired resistance, difficulties arise in attempting to assign significance to non-humoral factors even though they may represent the major component of the host's defense mechanism.A series of studies has been undertaken to analyse the mechanism of acquired resistance to a facultative intracellular parasite, and the immunological processes upon which it is based. It was realised at the outset that this would be possible only if the combination of host and parasite was chosen so that technical problems were minimised, and the immune state were efficient enough to make its demonstration possible in vitro.The present series of investigations deal with the pathogenesis of listeriosis in mice. The course of the investigation was dictated by several considerations: that non-humoral immunity could express itself in a pure form only against a true facultative intracellular parasite; that the mouse develops a true acquired resistance to Lisleria (6); and that resistance to Lisleria monocytogenes is not 381 on

Retracted: α‐GalCer ameliorates listeriosis by accelerating infiltration of Gr‐1+ cells into the liver

“…Thus, inflammation in the spleen and liver was prevented by a-GalCer in an iNKTcell-dependent manner. During systemic infection, a vast majority of L. monocytogenes microorganisms are first trapped in the liver [23] and iNKT cells are abundant in the liver [37,38]. Therefore, we focused on the liver in the following experiment.…”

“…monocytogenes infection [19][20][21][22]. The vast majority of L. monocytogenes organisms are trapped in the liver immediately after systemic infection [23] and hence, immunocompetent cells that reside in, and/or migrate into, the liver are critical for infection control.NKT cells represent a unique subset of T lymphocytes, which are characterized by the co-expression of NK cell markers such as NKR-P1B/C (NK1.1; CD161) [24]. In the mouse, the majority of NKT cells express an invariant (i) TCR composed of Va14/Ja18 gene segments, i.e.…”

“…monocytogenes infection [19][20][21][22]. The vast majority of L. monocytogenes organisms are trapped in the liver immediately after systemic infection [23] and hence, immunocompetent cells that reside in, and/or migrate into, the liver are critical for infection control.…”

The Functional Heterogeneity of Macrophages at the Single Cell Level

“…The strains of bacteria used in these studies were Sahrumella typhimurium C5 resistant to 500 (ig./nil. streptomycin, Salmonella enteritidis llRX (Ushiba, Saito, Akiyama, Nakano, Sugiyamo and Shirono, 1959), Listeria monocytogenes (Mackaness, 1961) resistant to 10 ng./nil. streptomycin and peniciUin.…”

Host Responses and Antigens Involved in Protective Immunity to Mycobacterium tuberculosis

“…The AG 85 complex (30)(31)(32). This group of outer cell wall antigens consists of three distinct, although markedly crossreacting, components denoted AG85A, B and C (reviewed by Wiker and Harboe, ref.…”