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The ability of serum complement to kill bacteria has been linked to host resistance to Gram-negative bacteria. A mechanism for killing extracellular organisms during early invasion, following release from infected phagocytic cells, or during bacteremia would contribute to a host's ability to resist disease. In fact, the ability of serum complement to kill bacteria has been linked to disease resistance. Brucella abortus are Gram-negative intracellular pathogens. Resistance to these bacteria involves the coordinated activities of the cellular and humoral immune systems. The existence of serum-resistant forms of B. abortus has been established, and it has been shown that these bacteria can resist the killing action of complement even in the presence of specific antibody. Antibody is usually necessary for complement-mediated killing of smooth (virulent) forms of Gram-negative bacteria. An anomolous situation exists with some isolates of smooth B. abortus. Sera containing high titers of specific antibody do not support killing unless they are diluted. In the bovine, this phenomenon is associated with IgG1 and IgG2 antibodies. This finding may account for the lack of positive correlation between antibody levels and resistance to disease, which has led, perhaps wrongly, to the idea that antibody and complement are not important in resistance to brucellosis. Available evidence suggests that antibody may have contradictory roles in the interactions between a host and bacteria. Avirulent (rough) forms of the organism would be rapidly killed by complement shortly after invasion, but serum-resistant smooth forms of the organism would survive and invade resident phagocytic cells. During the process of invasion and phagocytosis, the bacteria would initiate an immune response. With time, some B. abortus organisms would be released from infected phagocytic cells. In the early stages of this process, the bacteria would encounter IgM antibody and low concentrations of IgG antibody. These would cause complement-mediated killing, and infection would be restricted to resident phagocytic cells. However, the immune response to B. abortus antigens would be intensified, and IgG antibody levels would increase. High concentrations of antibody do no support complement-mediated killing of extracellular B. abortus, but the bacteria would be opsonized by antibody and complement component fragments. This would lead to increased phagocytosis of extracellular B. abortus as they appear, and concomitant extension of disease. Because of high levels of antibody would block complement-mediated killing of B. abortus, resistance to disease at this point would be dependent on cell-mediated immunity.

Prestalk and prespore cells form a simple pattern in the pseudoplasmodium of the cellular slime mold Dictyostelium discoideum. Prestalk cells are distinguished from prespore cells by a low level of expression of a glycoantigen on their surfaces and by reduced intercellular cohesion. We examined the possible significance of these differences, using the modB mutation, which eliminates this glycoantigen genetically, leading to reduced intercellular cohesion. The formation of patterns of cells during development is essential to tissue morphogenesis. The cells in the pseudoplasmodium (or slug) of the cellular slime mold Dictyostelium form a pattern consisting of prestalk cells, which lie in the anterior 20-30% of the slug, and prespore cells, which lie in the remaining portion (1, 2). Mixed with the prespore cells is a small proportion (ca. 10%) of cells that most resemble prestalk cells but do not behave in the same way; these are referred to as anterior-like cells (3). Slugs form as the result of aggregation of cells after starvation and their rearrangement into a slug-shaped structure. During this phase, all cells appear to be the same biochemically and morphologically. However, evidence has accumulated that cells are determined to become prestalk or prespore cells at the time of starvation according to the phase of the cell cycle (4-6) and their glycogen content (7). These findings support the general model that cells first differentiate (8) and then rearrange themselves (3, 9-12), either by "self-assembly" (13) or with the help of a tip-localized organizer (14, 15). The mechanism of this rearrangement remains obscure, with evidence for both differential cell adhesion (16, 17) and cheniotaxis (18) having been presented.Determination in Dictyostelium is reversible. For example, raising the temperature in strains carrying a temperaturesensitive (ts) allele of stkA directs prespore cells to transdifferentiate into prestalk cells (19,20). Simple amputations cause morphallactic transdifferentiation of prestalk into prespore cells and vice versa (21). A diffusible substance (DIF) appears to act in the slug to influence prestalk-cell differentiation (22). In Dictyostelium mucoroides, prespore cells continuously transdifferentiate into prestalk cells as they traverse a boundary near the anterior end of the slug (23). Perhaps an initial process of deterministic differentiation and cell sorting serves to set up a provisional pattern, which is followed by a regulative phase guided by a positional component.In this report we examine the behavior of modB mutant cells introduced into normal slugs and vice versa. The modB mutation exerts a relatively limited effect on protein glycosylation: only two of the six glycoantigens (GAgs; defined at least in part by carbohydrate) we have screened are affected, and reactivity with mannose-and GIcNAc-reactive lectins is not dramatically altered (refs. 24 and 25; data not shown). The affected GAgs (GAg-XI and GAg-XX) are normally expressed only in aggregation stage cells and later...

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