In summary, research in neuroimmunology over the last four decades has
shown that there are many interactions between the nervous and the immune
system. Neuroimmune interactions can be studied at different levels in the
organism (from molecules to systems and even with an attention to environ-
mental influences), at different scales (some neuroimmune communication
pathways are short-distance, others are long-distance), and through an attention
to different routes (direct interactions, but also indirect interactions, such as
those involving endocrine elements or the microbiota).
5.3 Interactions between the Nervous and the Immune
System in Pathological Contexts
According to some authors, neuroimmune interactions play a role not only in
physiological but also in pathological contexts. Many disorders classically
defined as neuronal and/or psychiatric are now said to possess a significant
immunological component (Kipnis 2016). This is the case, for example, for
some neurodegenerative disorders (Heneka et al. 2014) such as multiple sclero-
sis, which is an autoimmune disease (Dendrou et al. 2015), but also in
Alzheimer’s disease (Heppner et al. 2015). In addition, several lines of evidence
suggest that various psychiatric pathologies could be caused, at least in part, by
components of the immune system. Some authors emphasize that antineuronal
autoantibodies are found in the serum of 11.6 percent of 925 patients admitted to
acute psychiatric inpatient care (Schou et al. 2016), others that 20 to 40 percent
of acute psychiatric inpatients exhibit low-grade inflammation, suggesting the
possibility that inflammation can be relevant for many psychiatric disorders
(Osimo et al. 2018) (as typically recognized for schizophrenia (Khandaker et al.
2015)). Many of these observations are limited and only correlative, so more
work is needed to draw any conclusion here. An additional layer of complexity
is that some autoimmune diseases such as lupus are accompanied with neurop-
sychiatric manifestations, which may be due to the existence of brain-reactive
autoantibodies (Williams et al. 2010).
Several researchers propose that the immune system plays an important role
in major depressive disorder. In humans, one-third of patients treated with
cytokine therapies (IL-2 and IFN-α) for cancer or chronic viral hepatitis develop
major depressive disorders (Raison et al. 2006). Clinical observations, epide-
miological studies, and investigations in animal models have tended to confirm
that pro-inflammatory cytokines can induce depressive-like behaviors (Dantzer
et al. 2008). All this has contributed to the development of a non–brain-centric
view of depression. The causal involvement of indoleamine 2,3-dioxygenase
(IDO), an immune-inducible enzyme that metabolizes tryptophan along the
52 Elements in the Philosophy of Biology