The similarity between neural and (adaptive) immune networks has been known for decades, but so far we did not understand the mechanism that allows the immune system, unlike associative neural networks, to recall and execute a large number of memorized defense strategies in parallel. The explanation turns out to lie in the network topology. Neurons interact typically with a large number of other neurons, whereas interactions among lymphocytes in immune networks are very specific, and described by graphs with finite connectivity. In this paper we use replica techniques to solve a statistical mechanical immune network model with 'coordinator branches' (T-cells) and 'effector branches' (B-cells), and show how the finite connectivity enables the coordinators to manage an extensive number of effectors simultaneously, even above the percolation threshold (where clonal cross-talk is not negligible). A consequence of its underlying topological sparsity is that the adaptive immune system exhibits only weak ergodicity breaking, so that also spontaneous switch-like effects as bi-stabilities are present: the latter may play a significant role in the maintenance of immune homeostasis.Beyond the so-far-classical approaches by Cohen, DeBoer, May, Nowak and Perelson (see e.g. [1,2,3,4,5]) that paved the main route for mathematical modelling in Immunology, and after a pioneering early paper by Parisi [6] followed by about two decades of dormancy, there is now increasing interest in statistical mechanical approaches to modeling the immune system [7,8,15,13,14,9,10,11,12,16]. This interest is stimulated in part by the potential of new quantitative methods for the study of systems with complex network topologies [18,19,20,21,17]. In this paper we show how statistical mechanics can resolve a central problem in theoretical immunology: understanding the parallel processing ability of the subclass of lymphocytes that are dedicated to the coordination of the adaptive immune response, i.e. helper and regulator T-cells.T-and B-lymphocytes are divided into clones. Cells of the same B clone detect and attack the same antigens, and are selected for activation when their allocated antigens invade the host. Conditional on authorization by T-helpers (via eliciting cytokines), the selected B-cells undergo clonal expansion: they multiply, and start releasing high quantities of soluble antibodies to inhibit the enemy. After the antigen has been deleted, B-cells are no longer triggered, thus -instructed by T-regulators (via suppressive cytokines)-stop producing antibodies and undergo apoptosis. In this way the clones reduce their sizes, and order is restored. We stress that two signals are required for B-cell clones to expand. The first arises from antigen binding; the second is a 'consensus' signal, a cytokine secreted by T-helpers. This AND-gate like mechanism [29,30] prevents abnormal reactions, such as autoimmunity [22,7]. The core of the immune adaptive response thus consists of an effector branch (the B-clones 1 ) and a coordination branch (th...