| | Immunoescape mechanism | Details | References |
| | Structural/antigenic variation | It consists in the modified expression of domains, which are antigenically different within a clonal population, by which the pathogen is able to escape the host immunity selection and circumvent the immune surveillance
It usually involves LOS/LPS, opacity, and pilin proteins
LOS/LPS and opacity factor structural/antigenic variation depends essentially on phase variation
Pili antigenic variations depend on RecA-mediated recombination |
[31, 75, 76] |
| | Autolysis | It is mediated by OMPLA | [77] |
| | Blebbing and microvesicles formation | The blebs originate as evaginations of the outer layer | [78] |
| | Capsule switching | Due to microevolution, there is shift from serogroup B to serogroup C, from serogroup C to W-135, from serogroup Y to W-135, and from serogroup Y to B; nanostructured materials such as MWNTs and mesoporous silica increase transformational capacity | [30, 79–87] |
| | Capsule modification | For example, modification of lipid A of meningococcal LOS/LPS with phosphoethanolamine protects Neisseria from neutrophils-mediated killing
Another example is given by the O-acetylation of capsular antigens (LpxL2 gene mutants are indeed more virulent)
LpxL1 gene mutants activate TLR4 less efficiently | [88] |
| | Genome plasticity | HGT/LGT (via conjugation, transduction, and transformation) and homologous intragenic recombination | [25, 27, 30, 89] |
| | Host modification | Neisseria exploits a bacterial sialyltransferase scavenging available host CMP-NANA for modifying LOS/LPS | [70] |
| | Molecular mimicry | CP of serogroup B strain is a homopolymer of α2-8-linked sialic acid and is similar to NCAM-1
L-NNT in the lipopolysaccharide of virulent strains is similar to an antigen on red blood cells
DMP19 acts as a DNA-mimic protein | [67, 69, 71–74, 90, 91] |
| | Metabolic pathways | Examples are iron, lactate, glutamate uptake, utilization, and avoidance of neutrophil oxidation burst, ROS, and RNS | [92, 93] |
| | Molecular decoy | FprB has an antigenic subdomain for binding antibodies, which is not essential for the functioning of the autotransporter; it also blebs with OMPs and LPS/LOS distract the immune system, directing the response away from the microbe | [94] |
| | Immunotype switch | LPS immunotype switches from L3 to L8/L1 by lgtA, lgtC phase variation
LOS immunotype can contribute to immunoescape | [95, 96] |
| | Phages and prophages | The pathogen hosts a number of prophages, from the Mu-related family to the phage l-related group and the family of filamentous M13-like phages | [25, 30, 89]
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| | Phase variation | High-frequency reversible changes can occur in the length of SSRs (of capsule, LOS, opacity factor, porin, adhesin, invasin, autotransporter, haemoglobin receptor, DNA mismatch repair, and pilin genes, termed as contingency genes and organized in modules called phasevarions)
Other repeat sequences can be REP2, CRs, CREEs, and NIMEs
Transposon-like elements can play a role
Phase variation mediates resistance to antibiotics
Phase variation mediates carriage persistence | [50, 52, 59] |
| | Pilin conversion and modification | Pilin is posttranslationally modified by addition of a glycan, two phosphorylcholines, and a glyceramido acetamido trideoxyhexose residue | [97, 98] |
| | Plasmid | Examples of plasmids that can contribute to Neisseria variability are pJS-A, pJS-B | [33] |
| | Recruitment of human components of immune system | Neisseria escapes complement-mediated killing recruiting and sequestering fH to its surface | [91] |
| | Temperature-regulated defence | RNA thermosensors finely tune the expression of CP components, LOS, and fHBP, thus protecting against human immune killing | [99] |
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